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A statistical comparison of two human genomes

In a previous post I provided a statistical test to compare chimpanzee and human genomes. As you can read there, the post generated a very interesting discussion among the readers, and it seemed to me that the general feeling at the end was that my statistical method for performing genome-wide comparisons might have some merit, after all.

One reader suggested applying an identical test in order to compare two human genomes. That sounded like a very good idea to me, so I downloaded another human genome dataset from NCBI and performed a test.

For the benefit of readers, I’ll briefly recapitulate the simple comparison algorithm used in my previous test. 10,000 different sequences, each composed of 30 consecutive DNA bases (possible values: A, T, G and C) were randomly selected from chromosome N of genome A. A search for a matching pattern was then performed on the corresponding chromosome N of genome B. A pattern match was deemed to occur only when all 30 base pairs coincided perfectly – in other words, the head-to-head comparison between these DNA sub-strings was not relaxed, as occurs in many other tests in evolutionary comparative genomics. The total number of pattern matches found for that particular chromosome was then recorded. All chromosomes were tested in a similar fashion. Readers can view the latest results in the table and chart below, and compare them with the earlier results for the chimpanzee vs. human comparison.

As expected, the number of pattern matches was always significantly greater when comparing two humans than when comparing a chimpanzee with a human. As the chart above clearly shows, the number of matches in human vs. human comparisons was quite stable, ranging from 9507 to 9705 (chromosome Y is the sole exception, with 8989). However, the same did not hold for chimpanzee vs. human comparisons, where the values were much more scattered.

Finally, the average number of pattern matches per chromosome, shown at the bottom of the table, was very different in the two cases: 9616 for human vs. human comparisons, but only 6173 for chimp vs. human comparisons. The average number of patterns without a match for human vs. human comparisons was (10000 – 9616) = 384, or in percentage terms, 384/10000 = 3.84%. The average number of patterns without a match in human vs. chimp comparisons was (10000 – 6173) = 3827, or in percentage terms, 3827/10000 = 38.27%, which is almost ten times greater.

So the bottom-line question is: if, as many evolutionists say, chimpanzee and human genomes are 99% identical, how “identical” are two human genomes?

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130 Responses to A statistical comparison of two human genomes

  1. Thanks, this is a very interesting post. Couple of questions, as I’m kind of new to this area:

    Could you tell us a bit more about how the matches are done (it may be in your previous post, but the link doesn’t work).

    Also, when you say that the differential was 384/10000 for humans, is that base pair hits, identified gene coding sequences, etc.? Does it take into account moves, introns, etc.?

    I thought the early chimp comparison was done by breaking up the dna and seeing how much recombined with chimp dna, yielding a very high (but very suspect) number. Based on your numbers above, could one argue that a chimp is only 61% similar, or do your numbers point to something else?

  2. I think an accepted percent difference between humans is 0.1-0.2%, so the 30bp metric works really consistently. If you divide the 30bp metric by 3.84% by 24 you get .16% and 38.27 by 24, it is 1.59%. As mismatches increase, the 30bp metric might tend to underestimate, as a 2 nt difference in a 30 nt string still produces a mismatch. But for highly similar targets, it seems like a pretty fast and effective test.

  3. Last post had a bad typo:

    I think an accepted percent difference between humans is 0.1-0.2%, so the 30bp metric works really consistently. If you divide the 30bp metric of 3.84% by 24 you get .16%. Similarly, 38.27 divided by 24 is 1.59%. As mismatches increase, the 30bp metric might tend to underestimate, as a 2 nt difference in a 30 nt string still produces a mismatch. At this level, there will probably be zero matches anyway. But for highly similar targets, it seems like a pretty fast and effective test.

  4. So the bottom-line question is: if, as many evolutionists say, chimpanzee and human genomes are 99% identical, how “identical” are two human genomes?

    Well, what you’ve said above is not a quote from the researchers involved.

    From NIH on the topic in 2005:“The consortium found that the chimp and human genomes are very similar and encode very similar proteins. The DNA sequence that can be directly compared between the two genomes is almost 99 percent identical. When DNA insertions and deletions are taken into account, humans and chimps still share 96 percent of their sequence. At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans. In fact, the typical human protein has accumulated just one unique change since chimps and humans diverged from a common ancestor about 6 million years ago.”

    Emphasis added.

    Source.

  5. You mentioned in your two posts the sources of your two human genomic data sets. Do you have any information which would indicate how closely those two sets might reflect a similar genetic background? I.E. were they both white western Europeans?

    I think this is really interesting but I’d like to see more comparisons run with many different human genome datasets. One comparison does not a hypothesis make. Twenty comparisons is starting to establish a case. One hundred comparisons just might be establishing a paradigm.

    Also, it would be interesting, if your metric proves valuable, to compare chimps and gorillas and orangutangs and humans to see if the similarity analysis matches the consensus tree of descent.

    Sounds like a good area of ID research!!

  6. As to paulmc trying to assert that gene and protein sequences between chimps and humans are virtually identical, I would like to point out that evolutionists have severely distorted this particular line of evidence to fit their preconceived bias:

    There are over 1000 completely unique ‘ORFan’ genes, not found in any other known species, intertwined in the 22,000 genes of the human genome:

    Human Gene Count Tumbles Again – 2008
    Excerpt: Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences.
    http://www.sciencedaily.com/re.....161406.htm

    The authors of the preceding study tried to ‘remove the unique genes’ from the human gene catalog simply because they could not find matches in any supposed precursor species, and not for any lack of functionality on the genes part. This following site has a brief discussion on that biased methodology of the preceding study:
    http://www.uncommondescent.com.....ent-358505

    Moreover the ‘anomaly’ of unique ORFan genes is found in every new genome sequenced thus far:

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    As well, completely contrary to evolutionary thought, these ‘new’ ORFan genes are found to be just as essential as ‘old’ genes for maintaining life:

    Age doesn’t matter: New genes are as essential as ancient ones – December 2010
    Excerpt: “A new gene is as essential as any other gene; the importance of a gene is independent of its age,” said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. “New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked.”
    http://www.sciencedaily.com/re.....142523.htm

    I would like to reiterate that evolutionists cannot account for the origination of even one unique gene or protein, much less the over one thousand completely unique ORFan genes found distinctly embedded within the 20,000 genes of the human genome:

    Protein Folding and Evolution – December 2010
    Excerpt: A typical gene has something like a thousand nucleotides. Given that there are four different types of nucleotides, this means there are 4^1000 different sequences that could make up the gene. This is equal to a 1 followed by about 600 zeros—a big number. That’s more than the number of nano seconds since the Big Bang—by about 10^574 (a 1 followed by 574 zeros). Finding the right gene sequence to get a particular job done in the cell would make finding a needle in a haystack seem easy. The problem is so difficult that we haven’t yet figured out the answer, but it would be a 1 in 10^100++ long shot. Do not try this at home.
    http://darwins-god.blogspot.co.....ution.html

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

    “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: – Doug Axe ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.”
    http://www.mendeley.com/resear.....yme-folds/

    So where did these completely unique genes come from and why are neo-Darwinists so disposed to ignore them??? i.e. why are we continually sold a bill of goods as to the actually evidence by neo-darwinists???

    ,,, and this tidbit that just came out last week is also of interest:

    New level of genetic diversity in human RNA sequences uncovered
    Excerpt: They call these sites RNA-DNA differences, or RDDs. They found at least one RDD site in about 40 percent of genes, and many of these RDDs cause the cell to produce different protein sequences than would be expected based on the DNA. In the cells they studied, the sequences of thousands of proteins may be different from their corresponding DNA, the scientists say.
    http://www.physorg.com/news/20.....ences.html

    My hunch is that these RNA sites are drastically different between chimps and man as well???

  7. ellazimm, and I would like to see just where kangaroos fall on that tree:

    Evolutionists were recently completely surprised by this genetic study of kangaroos:

    Kangaroo genes close to humans
    Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
    http://www.reuters.com/article.....P020081118

    I’m just left wondering exactly where evolutionists should place the kangaroos on their cartoon drawings that show man evolving from apes.

  8. BA77: I’d like to see the whole ‘tree’ of life subjected to the best and most recent genetic analysis, kangaroos included!

    I LIKE DATA!!

    I’ll try and track down a good graphic showing how humans and marsupials fit into common descent based on the predominant view.

  9. It’s interesting looking for good graphical representations of common descent. And humbling to realise how much time and effort has been put into the research behind this:

    http://upload.wikimedia.org/wi.....edTree.jpg

  10. why ellazimm here you go Darwin’s tree of life is ‘annihilated :

    Here is another article, written by an evolutionist mind you, that states the true pattern found for life, from comparative genetic evidence, is not the tree pattern Darwin had envisioned:

    A New Model for Evolution: A Rhizome – May 2010
    Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations.
    http://darwins-god.blogspot.co.....izome.html

    “Why Darwin was wrong about the tree of life,” New Scientist (January 21, 2009)
    Excerpt: “Phylogenetic incongruities [conflicts] can be seen everywhere in the universal tree, from its root to the major branchings within and among the various taxa to the makeup of the primary groupings themselves.”,,, “We’ve just annihilated the (Darwin’s) tree of life.”
    http://www.evolutionnews.org/2......html#more

    More Questions for Evolutionists – August 2010
    Excerpt: First of all, we have 65% of the gene number of humans in little old sponges—an organism that appears as far back as 635 million years ago, about as old as you can get [except for bacteria]. This kind of demolishes Darwin’s argument about what he called the pre-Silurian (pre-Cambrian). 635 mya predates both the Cambrian AND the Edicarian, which comes before the Cambrian (i.e., the pre-Cambrian) IOW, out of nowhere, 18,000 animal genes. Darwinian gradualism is dealt a death blow here (unless you’re a ‘true believer”!). Here’s a quote: “It means there was an elaborate machinery in place that already had some function. What I want to know now is what were all these genes doing prior to the advent of sponge.” (Charles Marshall, director of the University of California Museum of Paleontology in Berkeley.) I want to know, too!
    http://www.uncommondescent.com.....utionists/

    Since evolutionists continually misrepresent the true state of the evidence for molecular sequences, here are several more comments and articles, by leading experts, on the incongruence of molecular sequences to Darwin’s theory:
    https://docs.google.com/document/pub?id=1S5wXsukzkauD5YQLkQYuIMGL25I4fJrOUzJhONvBXe4

    =======

    Primate Phylogenetics Challenge Darwin’s Tree of Life – Casey Luskin – audio podcast
    http://intelligentdesign.podom.....2_00-07_00

    A False Trichotomy
    Excerpt: The common chimp (Pan troglodytes) and human Y chromosomes are “horrendously different from each other”, says David Page,,, “It looks like there’s been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages.”
    http://www.uncommondescent.com.....richotomy/

    The Unbearable Lightness of Chimp-Human Genome Similarity
    Excerpt: One can seriously call into question the statement that human and chimp genomes are 99% identical. For one thing, it has been noted in the literature that the exact degree of identity between the two genomes is as yet unknown (Cohen, J., 2007. Relative differences: The myth of 1% Science 316: 1836.). ,,, In short, the figure of identity that one wants to use is dependent on various methodological factors.
    http://www.evolutionnews.org/2......html#more

  11. BA77: Is there a major refutation to neo-Darwinism if the ‘tree’ of life is more of a rhizome?

    From the source paper:

    “A post-Darwinist concept of the living species can be proposed, to integrate the theories of multiplicity and de-novo creation … I believe that the evolution of species looks much more like a rhizome (or a mycelium). Consequently, this view of evolution resembles a clump of roots that considers the occurrence of multiplicities. Emerging species grow from the rhizome with gene repertoires of various origins that will allow, under favourable environmental conditions, the multiplication and perpetuation of this species. As such, potential new species and new genes are continuously appearing.”

    A clump of roots but not species appearing with no antecedents.

    I do appreciate your links and references but mostly they are to ID favourable blogs or websites. I know those blogs and websites are referencing mainstream research but I think it’s important to look at the source material and its interpretation by the majority of people working in the field. It’s important to consider all the data and all the interpretations.

  12. paulmc @4: “At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans.”

    Just trying to figure out what this means. Does it mean that 61% of our genes code for different amino acid sequences than in chimps?

  13. Eric-”paulmc @4: “At the protein level, 29 percent of genes code for the same amino sequences in chimps and humans.”

    Just trying to figure out what this means. Does it mean that 61% of our genes code for different amino acid sequences than in chimps?”

    It means 29% of the protein coding genes are identical at each and every amino acid. The rest differ usually only at a single amino acid (out of hundreds).

  14. DrREC and ellazimm, you guys have either willingly, or have been deceived into buying into perhaps the shoddiest science in history, of there actually being a coherent ‘tree of life’ for neo-Darwinism from genetic similarities alone,,, i.e. the only way a ‘tree’ emerges from genetic data sets is if neo-Darwinism is assumed to be true in the first place and then computers are programmed to ‘find’ that unproven assumption,, all the while ignoring all dis-confirming sequences,,,

    Pattern pluralism and the Tree of Life hypothesis – 2006
    Excerpt: Hierarchical structure can always be imposed on or extracted from such data sets by algorithms designed to do so, but at its base the universal TOL rests on an unproven assumption about pattern that, given what we know about process, is unlikely to be broadly true.
    http://www.pnas.org/content/104/7/2043.abstract

    A Primer on the Tree of Life – Casey Luskin – 2009
    Excerpt: The truth is that common ancestry is merely an assumption that governs interpretation of the data, not an undeniable conclusion, and whenever data contradicts expectations of common descent, evolutionists resort to a variety of different ad hoc rationalizations to save common descent from being falsified.
    http://www.discovery.org/a/10651

    ,,, Moreover you guys have completely forgotten that you have no scientific basis in which to rest your evidence for genetic similarities, even if you had such ‘suggestive similarity evidence’ to start with; i.e you have NO FOUNDATIONAL MECHANISM from which to extrapolate your unwarranted conclusion,,, For instance,,,

    #1 both natural selection and random mutations reduce genetic information:

    Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) Casey Luskin April 12, 2011
    Excerpt; This is the issue I have with neo-Darwinists: They teach that what is generating novelty is the accumulation of random mutations in DNA, in a direction set by natural selection. If you want bigger eggs, you keep selecting the hens that are laying the biggest eggs, and you get bigger and bigger eggs. But you also get hens with defective feathers and wobbly legs. Natural selection eliminates and maybe maintains, but it doesn’t create….[N]eo-Darwinists say that new species emerge when mutations occur and modify and organism. I was taught over and over again that the accumulation of random mutations led to evolutionary change-led to new species. I believed it until I looked for evidence.
    http://www.evolutionnews.org/2.....45691.html

    Natural Selection Reduces Genetic Information – No Beneficial Mutations – Spetner – Denton – video
    http://www.metacafe.com/watch/4036816

    #2 neo-Darwinists have not even shown it to be possible to ‘fix’ a single beneficial mutation;

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

    Dr. Sanford calculates it would take 12 million years to “fix” a single base pair mutation into a population. He further calculates that to create a gene with 1000 base pairs, it would take 12 million x 1000 or 12 billion years. This is obviously too slow to support the creation of the human genome containing 3 billion base pairs.
    http://www.detectingtruth.com/?p=66

    Waiting Longer for Two Mutations – Michael J. Behe
    Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.
    http://www.discovery.org/a/9461

    #3 epigentics has falsified the ‘central dogma’ (modern synthesis) of neo-Darwinism, which is the premise that you are working from to try to establish genetic similarity as proof of common ancestry in the first place! i.e. you can mutate DNA till the cows come home and you will not effect body plan morphogenesis in any significant way!!!

    The Origin of Biological Information and the Higher Taxonomic Categories – Stephen Meyer
    “Neo-Darwinism seeks to explain the origin of new information, form, and structure as a result of selection acting on randomly arising variation at a very low level within the biological hierarchy, mainly, within the genetic text. Yet the major morphological innovations depend on a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. Yet if DNA is not wholly responsible for body plan morphogenesis, then DNA sequences can mutate indefinitely, without regard to realistic probabilistic limits, and still not produce a new body plan. Thus, the mechanism of natural selection acting on random mutations in DNA cannot in principle generate novel body plans, including those that first arose in the Cambrian explosion.”
    http://eyedesignbook.com/ch6/eyech6-append-d.html

    Getting Over the Code Delusion (Epigenetics) – Talbot – November 2010 – Excellent Article for explaining exactly why epigentics falsifies the neo-Darwinian paradigm of genetic reductionism:
    http://www.thenewatlantis.com/.....e-delusion

    etc.. etc…

  15. further notes:

    Stephen Meyer – Functional Proteins And Information For Body Plans – video
    http://www.metacafe.com/watch/4050681

    “Yet by the late 1980s it was becoming obvious to most genetic researchers, including myself, since my own main research interest in the ‘80s and ‘90s was human genetics, that the heroic effort to find the information specifying life’s order in the genes had failed. There was no longer the slightest justification for believing that there exists anything in the genome remotely resembling a program capable of specifying in detail all the complex order of the phenotype (Body Plan).”
    Michael John Denton page 172 of Uncommon Dissent

    This following study is very interesting for the researcher surveyed 130 DNA-based evolutionary trees to see if the results matched what ‘natural selection’ predicted for speciation and found:

    Accidental origins: Where species come from – March 2010
    Excerpt: If speciation results from natural selection via many small changes, you would expect the branch lengths to fit a bell-shaped curve.,,, Instead, Pagel’s team found that in 78 per cent of the trees, the best fit for the branch length distribution was another familiar curve, known as the exponential distribution. Like the bell curve, the exponential has a straightforward explanation – but it is a disquieting one for evolutionary biologists. The exponential is the pattern you get when you are waiting for some single, infrequent event to happen.,,,To Pagel, the implications for speciation are clear: “It isn’t the accumulation of events that causes a speciation, it’s single, rare events falling out of the sky, so to speak.”
    http://www.newscientist.com/ar.....tml?page=2

    The Biological Big Bang model for the major transitions in evolution – Eugene V Koonin – Background:
    “Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity. The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin’s original proposal, remains the dominant description of biological evolution. The cases in point include the origin of complex RNA molecules and protein folds; major groups of viruses; archaea and bacteria, and the principal lineages within each of these prokaryotic domains; eukaryotic supergroups; and animal phyla. In each of these pivotal nexuses in life’s history, the principal “types” seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate “grades” or intermediate forms between different types are detectable;
    http://www.biology-direct.com/content/2/1/21

    Biological Big Bangs – Origin Of Life and Cambrian – Dr. Fazale Rana – video
    http://www.metacafe.com/watch/4284466

  16. “i.e. the only way a ‘tree’ emerges from genetic data sets is if neo-Darwinism is assumed to be true in the first place and then computers are programmed to ‘find’ that unproven assumption,, all the while ignoring all dis-confirming sequences,,,”

    This is not true. For example, niwrad has developed a metric that definitively shows humans are more related to each other than chimps. I bet if he repeats the analysis with gorillas and orangutans he’ll be able to make a phylogenetic tree. Does it depend on trickery, or messing with the data?

    Does this paper, for example, pull some tricks I missed?

    A Molecular Phylogeny of Living Primates
    http://www.plosgenetics.org/ar.....en.1001342

  17. DrREC, does it not bother you in the least that you have no mechanism from which to extrapolate? since natural selection and random mutations both reduce genetic information??? Does it not bother you in the least that evolution cannot even explain the fixation of a SINGLE beneficial mutation??? Does it not bother you in the least that genetic reductionism (the central dogma), which is the entire neo-Darwinian premise you are working from, is falsified??? Does it not bother you in the least that over 1000 completely unique genes in humans were removed from consideration simply because no corresponding sequences could be found in any other primate or mammal??? ,,, So DRREC, I have shown you that you have no basis from which to work from scientifically, plus I have shown sheer intellectually dishonesty by neo-Darwinists in excluding completely unique genes in humans, but all this matters not to you and you pretend that if you can just find a study, any study, that shows sequences to match your preconceived conclusion then that will somehow overrule the fact that you have no foundation in the first place??? DrREC, this is science this is not Alice in wonderland!!! If you want to stay credible you must countermand the evidence I have marshaled that shows you to have no coherent mechanism for your conjectures!!!

  18. DrREC you state;

    I bet if he repeats the analysis with gorillas and orangutans he’ll be able to make a phylogenetic tree.

    Actually preliminary (hopefully unbiased) results are already in and you would lose that bet!!!

    Primate Phylogenetics Challenge Darwin’s Tree of Life – Casey Luskin – audio podcast
    http://intelligentdesign.podom.....2_00-07_00

  19. DrRec @ 13: “It means 29% of the protein coding genes are identical at each and every amino acid. The rest differ usually only at a single amino acid (out of hundreds).”

    OK, thanks. Just to make sure I’ve got my terminology correct, I think what you’re saying is not that 29% of the genes are necessarily identical at every base pair on the DNA, but that 29% of protein coding genes code for identical amino acids (presumably resulting in an identical protein, although that could be an interesting additional line of inquiry). That doesn’t necessarily mean that the gene is identical in all base pairs or in location, correct? In other words, there could be small differences at the DNA scale, but still result in the same amino acid sequence.

    For the other 61%, there are enough differences at the DNA level to result in at least one different amino acid in the chain. Presumably some (most?) of those would be due to different base pairs, but perhaps also there might be differences in introns, splicing, etc. that result in a different amino acid?

    Also interesting to know would be to what extent the different amino acid(s) result in a different functional protein. In other words, with a single different amino acid in the chain, I could presumably get: (i) a broken protein that doesn’t function, (ii) a protein that performs the same function, though not as well, (iii) a protein that performs the same function, just as well, or (iv) a protein that performs a completely different function.

    We haven’t of course focused at all on gene expression (timing and quantity), where I understand there are additional differences, and that is probably a topic for another time, but I just want to make sure I’m understanding the comparative approach that is being taken in looking at the gene-protein comparison.

  20. “DrREC, does it not bother you in the least that you have no mechanism from which to extrapolate?”

    Random mutation/recombination/gene duplication+ natural selection

    What is the mechanism of ID again?

    “since natural selection and random mutations both reduce genetic information???

    No.
    http://www.genetics.org/content/179/1/487.short
    http://genome.cshlp.org/conten......full.html
    http://www.ncbi.nlm.nih.gov/pubmed/18550802

    “Does it not bother you in the least that evolution cannot even explain the fixation of a SINGLE beneficial mutation??? ”
    http://www.ncbi.nlm.nih.gov/pu.....ion%20gene

    Results=6448

    “Does it not bother you in the least that genetic reductionism (the central dogma), which is the entire neo-Darwinian premise you are working from, is falsified??? ”

    Genetic reductionism is not the central dogma. Neo-Darwinian evolutionary biology is not the central dogma. I am not a neo-Darwinist.

    “completely unique genes in humans were removed from consideration simply because no corresponding sequences could be found in any other primate or mammal???”

    No. It was a reasonable approach. Unique genes can be added back if their transcription and expression can be verified by RNA/proteomic approaches. To my knowledge, 3 of these 1000 have been shown to be real genes.

    “pretend that if you can just find a study, any study, that shows sequences to match your preconceived conclusion then that will somehow overrule the fact that you have no foundation in the first place???”

    You should really investigate how molecular phylogenies are constructed. There is not bias loaded into the algorithms. Just pattern matching, parsimony and maximum likelyhood, backed by bootstrap and other statistical methods.

    “Actually preliminary (hopefully unbiased) results are already in and you would lose that bet!!!

    Primate Phylogenetics Challenge Darwin’s Tree of Life – Casey Luskin – audio podcast
    http://intelligentdesign.podom…..2_00-07_00″

    I’m not listening to 20 minutes of Luskin. Any salient point you’d like to condense and discuss? Or perhaps you’d like to perform a statistical analysis like the original post, and prove me wrong? The data sets and algorithms are available to the public.

  21. “OK, thanks. Just to make sure I’ve got my terminology correct, I think what you’re saying is not that 29% of the genes are necessarily identical at every base pair on the DNA, but that 29% of protein coding genes code for identical amino acids (presumably resulting in an identical protein, although that could be an interesting additional line of inquiry). ”

    Right-they’ll yield the same protein, thought the nucleotide differences could be interesting. A change at the nucleotide level could alter RNA stability, or transcription rate, or RNAi pairing, where there is no change at the protein level.

    “For the other 61%, there are enough differences at the DNA level to result in at least one different amino acid in the chain. Presumably some (most?) of those would be due to different base pairs, but perhaps also there might be differences in introns, splicing, etc. that result in a different amino acid?”

    Most of what we’re talking about here is a single base pair change that results in a different amino acid. There could be differential alternative splicing-but there is pretty limited data on that from many species.

    “Also interesting to know would be to what extent the different amino acid(s) result in a different functional protein. In other words, with a single different amino acid in the chain, I could presumably get: (i) a broken protein that doesn’t function, (ii) a protein that performs the same function, though not as well, (iii) a protein that performs the same function, just as well, or (iv) a protein that performs a completely different function.”

    Yep. Until tested biochemically, you wouldn’t know, though most proteins tend to be fairly robust to changes-so I’d bet on (iii) being more populated than (ii) and (i) which would be more abundant than (iv).

    “We haven’t of course focused at all on gene expression (timing and quantity), where I understand there are additional differences”

    And that is probably where the big differences in mammals are.

  22. DrREC,

    What is the mechanism of ID again?

    Intelligence!!!

    Alain Aspect and Anton Zeilinger by Richard Conn Henry – Physics Professor – John Hopkins University
    Excerpt: Why do people cling with such ferocity to belief in a mind-independent reality? It is surely because if there is no such reality, then ultimately (as far as we can know) mind alone exists. And if mind is not a product of real matter, but rather is the creator of the “illusion” of material reality (which has, in fact, despite the materialists, been known to be the case, since the discovery of quantum mechanics in 1925), then a theistic view of our existence becomes the only rational alternative to solipsism (solipsism is the philosophical idea that only one’s own mind is sure to exist). (Dr. Henry’s referenced experiment and paper – “An experimental test of non-local realism” by S. Gröblacher et. al., Nature 446, 871, April 2007 – “To be or not to be local” by Alain Aspect, Nature 446, 866, April 2007
    http://henry.pha.jhu.edu/aspect.html

    “since natural selection and random mutations both reduce genetic information???”

    The GS (genetic selection) Principle – David L. Abel – 2009
    Excerpt: Stunningly, information has been shown not to increase in the coding regions of DNA with evolution. Mutations do not produce increased information. Mira et al (65) showed that the amount of coding in DNA actually decreases with evolution of bacterial genomes, not increases. This paper parallels Petrov’s papers starting with (66) showing a net DNA loss with Drosophila evolution (67). Konopka (68) found strong evidence against the contention of Subba Rao et al (69, 70) that information increases with mutations. The information content of the coding regions in DNA does not tend to increase with evolution as hypothesized. Konopka also found Shannon complexity not to be a suitable indicator of evolutionary progress over a wide range of evolving genes. Konopka’s work applies Shannon theory to known functional text. Kok et al. (71) also found that information does not increase in DNA with evolution. As with Konopka, this finding is in the context of the change in mere Shannon uncertainty. The latter is a far more forgiving definition of information than that required for prescriptive information (PI) (21, 22, 33, 72). It is all the more significant that mutations do not program increased PI. Prescriptive information either instructs or directly produces formal function. No increase in Shannon or Prescriptive information occurs in duplication. What the above papers show is that not even variation of the duplication produces new information, not even Shannon “information.”
    http://www.bioscience.org/2009.....6/3426.pdf

    Falsification of Natural Selection
    https://docs.google.com/document/pub?id=10WqN_Z_2GjzhPQUVe7QmcMZDPObJCG45XqgF7pZVcVM

    ‘Does it not bother you in the least that evolution cannot even explain the fixation of a SINGLE beneficial mutation??? ”

    You cite quickly googled crap, and I cited the most rigorous study and mathematics available, and this is you being fair with the evidence to you DrREC???

    ‘Genetic reductionism is not the central dogma.’

    FALSE!!

    ‘I am not a neo-Darwinist.’

    FALSE!!

    “completely unique genes in humans were removed from consideration simply because no corresponding sequences could be found in any other primate or mammal???”

    No. It was a reasonable approach.

    FALSE!!

    “pretend that if you can just find a study, any study, that shows sequences to match your preconceived conclusion then that will somehow overrule the fact that you have no foundation in the first place???”

    You should really investigate how molecular phylogenies are constructed. There is not bias loaded into the algorithms.

    FALSE for a vast majority of neo-Darwinian studies!!!

    I’m not listening to 20 minutes of Luskin.

    YOUR LOSS!!!

    The Origin at 150: is a new evolutionary synthesis in sight? – Koonin – Nov. 2009
    Excerpt: The edifice of the modern synthesis has crumbled, apparently, beyond repair.
    http://www.arn.org/blogs/index....._synthesis

    Modern Synthesis of Neo-Darwinism Is Dead – Paul Nelson – video
    http://www.metacafe.com/watch/5548184/

  23. I’m not sure I should really indulge the avalanche of irrelevant links you think passes for debate, but I’m tempted to see how deep the rabbit hole goes….

    REC: “What is the mechanism of ID again?

    BA: Intelligence!!!”

    Intelligence is a noun. I was looking for a bit of verbage, I guess. “ID is not a mechanistic theory, and it’s not ID’s task to match your pathetic level of detail in telling mechanistic stories.” Right?

    BA: “The GS (genetic selection) Principle – David L. Abel – 2009″

    Abel is incomprehensible. Look at the Pubmed record for the article-he’s only been cited by himself. http://www.ncbi.nlm.nih.gov/pubmed/19273248
    Maybe it is interesting, but no one else has parsed it. Again, present the salient argument from the paper in your own words, and we’ll debate it.

    REC: “‘Genetic reductionism is not the central dogma.’

    BA: FALSE!!”

    Analysis? Or just shouting? What is the central dogma? What is genetic reductionism? Are they equivalent?

    REC: “‘I am not a neo-Darwinist.’

    BA: FALSE!!”

    You Know me better than myself? Interesting. Lol.

    BA: completely unique genes in humans were removed from consideration simply because no corresponding sequences could be found in any other primate or mammal???”

    REC: No. It was a reasonable approach.

    BA: FALSE!!

    No analysis. I defend the approach and describe its positive outcome above.

    REC: You should really investigate how molecular phylogenies are constructed. There is not bias loaded into the algorithms.

    BA: FALSE for a vast majority of neo-Darwinian studies!!

    Could you provide an example of a biased algorithm used to construct a phylogenetic tree? How was the bias programmed in?

    REC:I’m not listening to 20 minutes of Luskin.

    BA:YOUR LOSS!!!

    Again, please summarize the salient argument and we can debate it. I simply refuse to guess at the point you are trying to make in all these links. A key part of rational discussion is synthesis-where you take the facts, and present them in your own (concise) language. Spewing links is not dignified.

    Koonin is a premier evolutionary biologist. You’re quote mining quote mines.

    Is there anything relevant in the YEC Paul Nelson’s video? Or just another link to drown me with?

  24. DrREC:

    Thanks for the thoughts.

    “. . . most proteins tend to be fairly robust to changes . . .”

    Would it be fair to say that proteins are properly categorized by their function, rather than the specific sequence? I’m sure that is the case historically, as many functions were able to be discerned, but not the individual sequences. Do you know if there is any movement toward identifying proteins by specific sequence, or perhaps family of sequences that result in effectively the same protein? I’m wondering if, as we learn more and have a more complete database, we might ultimately start categorizing by specific sequence or at least having sub-categories for known variants which perform the same essential function.

    Also, my understanding was that additional error-correction mechanisms exist even in the translation stage (for example in the ribosome). Do we know if the ribosome ever identifies an “incorrect” amino acid and swaps it out for the correct one? In other words, is it possible that a change in a gene could result in a changed amino acid in a protein sequence, but we see the same functional protein produced and assume the amino acid change doesn’t matter, when in fact the amino acid was “corrected” prior to completion of the protein synthesis?

  25. BA77: In the Lynn Margolis interview you reference via a review by Casey Luskin she says:

    “All scientists agree that evolution has occurred – that all life comes from a common ancestry, that there has been extinction and that new taxa, new biological groups, have arisen. The question is, is natural selection enough to explain evolution? Is it the driver of evolution?”

    I’d reproduce more but I can’t copy-and-paste from the website, clever materialists! :-)

  26. Sorry, my bad, Lynn Margulis. I need more tea.

  27. Dr REC:

    In response to bornagain77, you wrote (#23):

    Abel is incomprehensible. Look at the Pubmed record for the article – he’s only been cited by himself. http://www.ncbi.nlm.nih.gov/pubmed/19273248

    Maybe it is interesting, but no one else has parsed it. Again, present the salient argument from the paper in your own words, and we’ll debate it….

    Again, please summarize the salient argument and we can debate it. I simply refuse to guess at the point you are trying to make in all these links. A key part of rational discussion is synthesis-where you take the facts, and present them in your own (concise) language. Spewing links is not dignified.

    May I refer you to your post #20, in which you “spew” four links. Here’s an excerpt from the first one at
    http://www.genetics.org/content/179/1/487.short :

    De Novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae

    Jing Cai, Ruoping Zhao, Huifeng Jiang and Wen Wang

    Abstract

    Origination of new genes is an important mechanism generating genetic novelties during the evolution of an organism. Processes of creating new genes using preexisting genes as the raw materials are well characterized, such as exon shuffling, gene duplication, retroposition, gene fusion, and fission. However, the process of how a new gene is de novo created from noncoding sequence is largely unknown. On the basis of genome comparison among yeast species, we have identified a new de novo protein-coding gene, BSC4 in Saccharomyces cerevisiae. The BSC4 gene has an open reading frame (ORF) encoding a 132-amino-acid-long peptide, while there is no homologous ORF in all the sequenced genomes of other fungal species, including its closely related species such as S. paradoxus and S. mikatae. The functional protein-coding feature of the BSC4 gene in S. cerevisiae is supported by population genetics, expression, proteomics, and synthetic lethal data. The evidence suggests that BSC4 may be involved in the DNA repair pathway during the stationary phase of S. cerevisiae and contribute to the robustness of S. cerevisiae, when shifted to a nutrient-poor environment. Because the corresponding noncoding sequences in S. paradoxus, S. mikatae, and S. bayanus also transcribe, we propose that a new de novo protein-coding gene may have evolved from a previously expressed noncoding sequence.

    Translation, please?

    One person’s “standard scientific terminology” is another person’s gibberish.

  28. DrREC you say you aren’t a neo-Darwinists yet you defend every precept they preach with as much, or more, vigor than many of them do. So what should I believe??? your actions or your empty words???

    This following site has a brief, and sobering, discussion on the extremely biased methodology of the “kick the ORFans genes out in the street” study:
    http://www.uncommondescent.com.....ent-358505

    ,,, DrREC, You tell more shallow falsehoods in defense of the other points, so I’ll go on to another point that is worth making;

    ,,, The claim going around is something like this ‘the proteins between chimps and humans are virtually the same but differ by only a few amino acids here and there’,,,, Yet do neo-Darwinists have foundation to make claim??? this study that came out just recently stated,,,

    Most Detailed Annotation of Fruit-Fly Genome Points Way to Understanding All Organisms’ Genomes – December 2010
    Excerpt: “We also found an order-of-magnitude increase in the ways that genes are spliced and edited to produce alternate forms of known proteins, thus significantly increasing the complexity of the proteome.”,,, Despite the scrutiny to which the Drosophila genome has been subjected, the researchers found new or altered exons or splice forms in almost three-quarters of Drosophila’s previously annotated genes,,,
    http://www.sciencedaily.com/re.....131131.htm

    ,,, from this preceding study, I am VERY certain that the neo-Darwinists are not giving us the straight scoop on protein dissimilarity between chimps and humans,,, indeed how can they possibly give us anything when they just discovered regulation that ‘significantly increased the complexity of the proteome.’,,,

    ,,,,as well as this testifies against the neo-Darwinists….

    New level of genetic diversity in human RNA sequences uncovered
    Excerpt: They call these sites RNA-DNA differences, or RDDs. They found at least one RDD site in about 40 percent of genes, and many of these RDDs cause the cell to produce different protein sequences than would be expected based on the DNA. In the cells they studied, the sequences of thousands of proteins may be different from their corresponding DNA, the scientists say.
    http://www.physorg.com/news/20.....ences.html

    ,,,Thus if they just discovered ‘thousands of new proteins’ that were completely different from what they expected from the DNA sequences alone, how in the world are neo-Darwinists justified in making the claim that virtually all chimp proteins are only a few amino acids different from human proteins or are the exact same, when they just discovered this???

    ,,, single genes are now shown to code for multiple ‘different’ protein products:

    Human genes are multitaskers:
    Abstract: Genome-wide surveys of gene expression in 15 different tissues and cell lines have revealed that up to 94% of human genes generate more than one (protein) product.
    http://www.nature.com/news/200......1199.html

    Human Genes: Alternative Splicing (For Proteins) Far More Common Than Thought:
    Excerpt: two different forms of the same protein, known as isoforms, can have different, even completely opposite functions. For example, one protein may activate cell death pathways while its close relative promotes cell survival.
    http://www.sciencedaily.com/re.....134623.htm

    This is particularly interesting,,,

    Researchers Crack ‘Splicing Code,’ Solve a Mystery Underlying Biological Complexity
    Excerpt: “For example, three neurexin genes can generate over 3,000 genetic messages that help control the wiring of the brain,” says Frey. “Previously, researchers couldn’t predict how the genetic messages would be rearranged, or spliced, within a living cell,” Frey said. “The splicing code that we discovered has been successfully used to predict how thousands of genetic messages are rearranged differently in many different tissues.
    http://www.sciencedaily.com/re.....133252.htm

    The preceding study put a ‘unique signature of individuality’ upon the human genome that sets it completely apart from the chimpanzee genome since functional ‘junk intron sequences’ were used in deciphering the ‘second genetic code’ (the splicing code),,,,

    Canadian Team Develops Alternative Splicing Code from Mouse Tissue Data
    Excerpt: “Our method takes as an input a collection of exons and surrounding intron sequences and data profiling how those exons are spliced in different tissues,” Frey and his co-authors wrote. “The method assembles a code that can predict how a transcript will be spliced in different tissues.”
    http://www.genomeweb.com/infor.....issue-data

    ,,, and yet these ‘junk intron sequences’, that were used to decipher the splicing code of different tissue types in an organism, are found to be ‘exceptionally different’ between chimpanzees and Humans:

    Modern origin of numerous alternatively spliced human introns from tandem arrays – 2006
    Excerpt: A comparison with orthologous regions in mouse and chimpanzee suggests a young age for the human introns with the most-similar boundaries. Finally, we show that these human introns are alternatively spliced with exceptionally high frequency.
    http://www.pnas.org/content/104/3/882.full

    This following paper is brutally honest as to what ignoring ‘Junk introns’ means for the future of molecular biology:

    Matheson’s Intron Fairy Tale – Richard Sternberg – June 2010
    Excerpt: The failure to recognize the importance of introns “may well go down as one of the biggest mistakes in the history of molecular biology.” –John Mattick, Molecular biologist, University of Queensland, quoted in Scientific American,,, So let’s do the math. At least ninety percent of gene transcripts undergo alternative splicing, and there are at least 190,000 introns in the human genome. That means we have at least 0.90 x 190,000 = 171,000 introns that participate in the alternative-splicing pathway(s) available to a cell.
    http://www.evolutionnews.org/2.....35301.html

    ,,,, etc.. etc.. etc.. continued falsification of all claims is just the way life is for neo-Darwinists, but don’t worry they will be back tomorrow forgetting everything they have been corrected on. The circus never ends! :)

  29. Thanks to all for the comments.

    Eric Anderson #1

    The test is purely statistical, it doesn’t take into account moves, introns, orphans and any functional concept. This is the reason why the test is so simple to do and, as DrREC noted, in the same time is fast and effective.

    About the difficulty of representing by a single number the genomic similarity you could read my previous post and all its comments (now the link works, thank you for alerting me of the fault).

    ellazimm #5

    I was unable to find in the data-banks the information about the race or country of the human genomes provided. I don’t exclude a-priori it exists somewhere.

  30. BA77: In the review of the study you site above, “Researchers Crack ‘Splicing Code,’ Solve a Mystery Underlying Biological Complexity” at Science Daily your seem to draw the following conclusions:

    “The preceding study put a ‘unique signature of individuality’ upon the human genome that sets it completely apart from the chimpanzee genome since functional ‘junk intron sequences’ were used in deciphering the ‘second genetic code’ (the splicing code),,,,”

    I could find no indication in the review that the researchers suggested that the splicing code they found was unique to humans (the study was done on human DNA) or any mention of ‘junk intron sequences’. In fact, if intron sequences were used I would think there would be a high probability that some of those sequences were also present in the chimp genome.

  31. BA77: The next review you site, “Canadian Team Develops Alternative Splicing Code from Mouse Tissue Data” may even be referencing the same bit of research. The names of the researchers are the same, the date the reviews were published is very close . . . . the first time I clicked on the link for the genomeweb review I was able to view the whole article but when I tried again I was blocked; I guess you have to pay! The second review clearly mentions mouse DNA whereas the first review does not actually say what DNA was used. (I was wrong earlier, human DNA is mentioned but not in association with the research.) And NOWHERE is it mentioned that this can be used to distinguish between human and chimp DNA.

    Also, neither of the reviews used the phrase “junk intron sequences”. In the excerpt you reproduce the researchers are quoted as saying “Our method takes as an input a collection of exons and surrounding intron sequences and data profiling how those exons are spliced in different tissues.”

    I’m not sure those two reviews actually make the point you want. Have a look again and see what you think.

  32. BA77: Continuing the quote you give from a paper reviewed at pnas.org:

    “Finally, we show that these human introns are alternatively spliced with exceptionally high frequency. Our study indicates that genomic duplication has been an important mode of intron gain in mammals. The alternative splicing of transcripts containing these intron-breeding repeats may provide the plasticity required for the rapid evolution of new human proteins.”

    Are you sure you want to use this reference?

  33. vjtorley: Translation, please?

    http://www.genetics.org/content/179/1/487.short :

    De Novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae

    New origination of a gene that codes for a protein in the yeast Saccharomyces cerevisiae

    Making new genes is an important way of generating novelties during the evolution of an organism. Making new genes from chunks of existing genes is well known, using processes such as shuffling the parts of existing genes, breaking parts off existing genes, joining two existing genes to make a new one, duplicating (and modifying) existing genes, etc.

    However, little is known about making a new gene “from scratch” using chunks of DNA that don’t code for a protein. By comparing the genomes of several different species of yeaste, the authors have identified a brand new gene, called BSC4 in the yeast Saccharomyces cerevisiae.

    The new BSC4 gene has a start codon followed by a stretch of DNA that codes for a 132 amino acid long peptide, which is a short piece of protein. This Open Reading Frame does not exist in any of the other fungal species that have had their DNA sequenced, including the closely related species Saccharomyces paradoxus and Saccharomyces mikatae .

    We know that the new BSC4 is a gene because we’ve detected the new protein that it makes. Population genetics,proteomics and synthetic lethal data also support this. (Not sure what that last one is.)

    The evidence shows that BSC4 may be involved in repairing DNA during the part of the yeast’s life cycle where it is not dividing. It also appears to make the yeast more likely to survive if shifted to a nutrient-poor environment.

    Because the same sequence in three other species of yeast are transcribed into peptides, we propose that BSC4 may be a brand new gene.

    Scientific papers do have translations. I don’t think you’ll be able to translate Dr. Abel’s paper. I’ve read it and as far as I can tell, it’s gibberish.

  34. ellazimm, last sentence you quoted states:

    ‘these intron-breeding repeats may provide the plasticity required for the rapid evolution of new human proteins.

    ,,, so do you concede that there are now shown to be ‘new human proteins’ that are unique to humans, that differ by more than a few amino acids from chimp proteins???

    If you do concede ‘new human proteins’, then besides just presuming that new proteins in humans evolved because they had to evolve because that is what you believe what happened, and making up a neo-Darwinian ‘just so’ story to fit that preconceived conclusion, how do actually explain ‘evolution’ finding a new functional sequence for these ‘new human proteins’????? i.e. ellazimm, not that I don’t appreciate such blind faith in the almighty power of Darwinism, but what is your foundational empirical support that purely random processes can actually find ‘new human proteins’ which are functional instead of just functionless protein junk???

    How Proteins Evolved – Cornelius Hunter – December 2010
    Excerpt: Comparing ATP binding with the incredible feats of hemoglobin, for example, is like comparing a tricycle with a jet airplane. And even the one in 10^12 shot, though it pales in comparison to the odds of constructing a more useful protein machine, is no small barrier. If that is what is required to even achieve simple ATP binding, then evolution would need to be incessantly running unsuccessful trials. The machinery to construct, use and benefit from a
    potential protein product would have to be in place, while failure after failure results. Evolution would make Thomas Edison appear lazy, running millions of trials after millions of trials before finding even the tiniest of function.
    http://darwins-god.blogspot.co.....olved.html

    Signature In The Cell – Review
    Excerpt: Even if you grant the most generous assumptions: that every elementary particle in the observable universe is a chemical laboratory randomly splicing amino acids into proteins every Planck time for the entire history of the universe, there is a vanishingly small probability that even a single functionally folded protein of 150 amino acids would have been created.
    http://www.fourmilab.ch/docume.....k_726.html

    Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe:
    Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.
    http://www.ncbi.nlm.nih.gov/pubmed/15321723

    Correcting Four Misconceptions about my 2004 Article in JMB — May 4th, 2011 by Douglas Axe
    http://biologicinstitute.org/2.....le-in-jmb/

    Extreme functional sensitivity to conservative amino acid changes on enzyme exteriors – Doug Axe
    Excerpt: Contrary to the prevalent view, then, enzyme function places severe constraints on residue identities at positions showing evolutionary variability, and at exterior non-active-site positions, in particular.
    http://nsmserver2.fullerton.ed.....lution.pdf

    Stability effects of mutations and protein evolvability. October 2009
    Excerpt: The accepted paradigm that proteins can tolerate nearly any amino acid substitution has been replaced by the view that the deleterious effects of mutations, and especially their tendency to undermine the thermodynamic and kinetic stability of protein, is a major constraint on protein evolvability,,
    http://www.ncbi.nlm.nih.gov/pubmed/19765975

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://biologicinstitute.org/2.....t-collide/

    ,,, ellazimm, when you remove the neo-Darwinian just so story for how new human proteins may have evolved, and look at the cold hard facts of science itself, finding a ‘new human protein’ is anything but the easy as pie story that neo-Darwinists portray it to be!!!

  35. OT; Here is a brand new Video on the molecular machinery of Protein Synthesis

    Protein synthesis (DNA transcription, translation and folding) – May 2011 – video
    http://www.youtube.com/watch?v=erOP76_qLWA

  36. Here is another question that will go unanswered by neo-Darinism,,,, How does the protein machine at the end of the preceding video (Chaperone) know exactly how to fold each unique protein into its proper, and unique, structure??? That machine, by itself, clearly displays ‘foresight and planning’ in molecular biology that is simply unavailable to neo-Darwinian processes.

    Chaperone (protein)
    Excerpt: However, ‘steric chaperones’ directly assist in the folding of specific proteins by providing essential steric information,
    http://en.wikipedia.org/wiki/C.....protein%29

  37. BA77: Well, the research examined human sequences with no attempt to compare them to chimp DNA.

    But I was more interested to note that purely mechanical processes seems to be adequate to the task of creating new human proteins. Or do you think someone has/will observe design in action?

    ” . . . how do actually explain ‘evolution’ finding a new functional sequence for these ‘new human proteins’??

    I explain it based on the work quoted in the study. That the plasticity is sufficient for the creation of new proteins. That’s why I was wondering why you were using it as support for your view. It sounds to me like it contradicts some of your beliefs.

    “How does the protein machine at the end of the preceding video (Chaperone) know exactly how to fold each unique protein into its proper, and unique, structure?”

    From Wikipedia: “Each protein exists as an unfolded polypeptide or random coil when translated from a sequence of mRNA to a linear chain of amino acids. This polypeptide lacks any developed three-dimensional structure. Amino acids interact with each other to produce a well-defined three-dimensional structure, the folded protein, known as the native state. The resulting three-dimensional structure is determined by the amino acid sequence ”

    Is that the sort of answer you wanted? The protein machine does no thinking, has no foresight.

    The whole paragraph from Wikipedia that you clipped a segment from:

    “Chaperones do not necessarily convey steric information required for proteins to fold: thus statements of the form ‘chaperones fold proteins’ can be misleading. One major function of chaperones is to prevent both newly synthesised polypeptide chains and assembled subunits from aggregating into nonfunctional structures. It is for this reason that many chaperones, but by no means all, are also heat shock proteins because the tendency to aggregate increases as proteins are denatured by stress. However, ‘steric chaperones’ directly assist in the folding of specific proteins by providing essential steric information, e.g. prodomains of bacterial proteases, lipase-specific foldases, or chaperones in fimbrial adhesion systems.”

    Thought I’d look up ‘steric’ as well:

    “Steric effects arise from the fact that each atom within a molecule occupies a certain amount of space. If atoms are brought too close together, there is an associated cost in energy due to overlapping electron clouds (Pauli or Born repulsion), and this may affect the molecule’s preferred shape (conformation) and reactivity.”

    I don’t see any intelligent processing going on, sorry.

  38. @ 24 Eric Anderson

    “Would it be fair to say that proteins are properly categorized by their function, rather than the specific sequence?”

    Sort of-for example, Enzymes are classified a few different ways. One is by their catalytic activity-this is the Enzyme Commission number. They can be classified by fold, and also by sequence.

    “I’m wondering if, as we learn more and have a more complete database, we might ultimately start categorizing by specific sequence or at least having sub-categories for known variants which perform the same essential function.”

    I would say that is ongoing in the way things are named. Take a histone methyltransferase-EC 2.1.1.43. We divide them into two folds-SET domain and non-SET (Dot1). Then subfamilies based on structural features and flanking domains. Then sequences into very related groups.

    “Also, my understanding was that additional error-correction mechanisms exist even in the translation stage (for example in the ribosome). Do we know if the ribosome ever identifies an “incorrect” amino acid and swaps it out for the correct one? In other words, is it possible that a change in a gene could result in a changed amino acid in a protein sequence, but we see the same functional protein produced and assume the amino acid change doesn’t matter, when in fact the amino acid was “corrected” prior to completion of the protein synthesis?”

    Ribosomes detect mispairing of tRNAs anticodons with the codon, and can eject the wrong tRNA. But usually what is on the mRNA is what enters the protein, for better or worse. Ribosomes don’t have the insight to correct genetically encoded mutations. One exception is nonsense suppression, where premature stop codons are read through by inserting some amino acid. In this case, it is the missing context of a genuine stop that allows the ribosome to keep making a product.

  39. “May I refer you to your post #20, in which you “spew” four links. Here’s an excerpt from the first one at
    http://www.genetics.org/content/179/1/487.short :

    De Novo Origination of a New Protein-Coding Gene in Saccharomyces cerevisiae”

    Sorry. I confess these ‘link wars’ do little for the discussion.

    In short, I was responding to BA77′s claim that origins of novel genes could not be accounted for. In this case, a transcribed RNA acquired mutations that led to the loss of in-frame stop codons that. The resulting protein provides a apparent fitness boost to one yeast, where the remainder of its close relatives seem to not make it. It shows strong signs of purifying selection.

    The other papers describe origins of genes in flies and humans, I believe.

  40. 28 bornagain77

    “,,, The claim going around is something like this ‘the proteins between chimps and humans are virtually the same but differ by only a few amino acids here and there’,,,, Yet do neo-Darwinists have foundation to make claim???”

    Both genomes are sequenced. You can do the BLAST searches yourself.

    How do Alternative splicing and RNA editing affect what we’re talking about here? niwrad has presented a metric for genomic similarity. Everyone knows transcriptional, post-transcriptional, and post-translational control will effect expression and diversity of products. This is not new.

    As for chaperones, they function by a very simple principle-hydrophobic amino acids belong on the inside of a protein, and hydrophilic on the outside. Chaperones tend to have high affinity for the extended and hydrophobic bits of an unfolded protein, and less affinity for the compact, folded bit. No foresight and imagination-just physical properties of protein folding.

    Steric chaperones are basically folding buddies for other proteins. Molecular recognition:

    “Several proteins do not fold correctly into their native structures without the help of steric chaperones. These chaperones imprint unique structural information onto target proteins while lowering the entropic (un)folding barrier between the native and partially folded states.”

    http://www.nature.com/nsmb/jou.....b1065.html

  41. 41

    “No foresight and imagination-just physical properties of protein folding.”

    Amazing that all those specific integrated parts just happen to be floating by at the right time. I think we could easily say that the stunning availability of bio-componentry is the most astonishing facet of Life, no?

    How supremely lucky for us all.

  42. Hmmm ellazimm, you state:

    ‘But I was more interested to note that purely mechanical processes seems to be adequate to the task of creating new human proteins.’

    FALSE!!! This is ‘just so’ asserted but is not demonstrated!

    Or do you think someone has/will observe design in action?

    When you wrote your post you watched ‘design in action’, in that you exceeded what is possible for the material processes of the universe over the entire history of the universe for the generation of functional information. Or do you want to claim you are not Intelligently Designing your posts???? Myself, that (your post) is another clear evidence that there is a ‘supernatural’ component to you that ‘transcends’ this material universe.

    ‘I explain it based on the work quoted in the study. That the plasticity is sufficient for the creation of new proteins.’

    FALSE!!! This is ‘just so’ asserted but is not demonstrated!

    you then state in regards to Chaperone:

    ‘Is that the sort of answer you wanted? The protein machine does no thinking, has no foresight.’

    The protein machine clearly demonstrates ‘teleology’ in its design. Teleological Design which requires the foresight of a designer to choose the correct path out of a nearly infinite number of incorrect paths;

    DrREC, as to your claim of brand new genes being created by purely material processes;

    De Novo Genes: Criticism From Nick Matzke
    Excerpt: At best it appears that evolution will be left with the usual “new proteins arise from the cutting, copying and pasting of pre existing proteins, with a few mutations thrown in here or there.” But that hardly makes a de novo gene, such as T-urf13, evidence that evolution creates new proteins.
    http://darwins-god.blogspot.co.....-nick.html

    So DrREC, does appealing to the unmatched levels of epigenetic information, in the genome, ‘calculating’ a ‘new’ protein/gene product in response to environmental stress constitute proof for that purely material processes of neo-Darwinism created the new gene and/or protein??? If you do accept this pathetic level of ‘proof’ it is clear that your religion of Darwinism is driving your science, But it was never about the science in the first place was it???

    Darwin’s Predictions – Cornelius Hunter – Religion drives science and it matters
    http://www.darwinspredictions.com/

    Failed Predictions of Evolutionists – Cornelius Hunter – audio
    http://intelligentdesign.podom.....0_49-08_00

    Science Owes Nothing To Darwinian Evolution – Jonathan Wells – video
    http://www.metacafe.com/watch/4028096

    You know what is crazy DrREC is that you act like you got any foundation at all to stand on in science. Whereas you, in reality, have nothing but circular rhetoric to deceive yourself with!! If you want to impress me, and rise above the contempt I have for your ‘snake oil’ salesman type of science. I suggest you change a bacteria into another species of bacteria by neo-Darwinian processes!!!

    Selection and Speciation: Why Darwinism Is False – Jonathan Wells:
    Excerpt: there are observed instances of secondary speciation — which is not what Darwinism needs — but no observed instances of primary speciation, not even in bacteria. British bacteriologist Alan H. Linton looked for confirmed reports of primary speciation and concluded in 2001: “None exists in the literature claiming that one species has been shown to evolve into another.”
    http://www.evolutionnews.org/2.....why_d.html

    The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland http://mbe.oxfordjournals.org/...../19/9/1637

    Static evolution: is pond scum the same now as billions of years ago?
    Excerpt: But what intrigues (paleo-biologist) J. William Schopf most is lack of change. Schopf was struck 30 years ago by the apparent similarities between some 1-billion-year-old fossils of blue-green bacteria and their modern microbial microbial. “They surprisingly looked exactly like modern species,” Schopf recalls. Now, after comparing data from throughout the world, Schopf and others have concluded that modern pond scum differs little from the ancient blue-greens. “This similarity in morphology is widespread among fossils of [varying] times,” says Schopf. As evidence, he cites the 3,000 such fossils found;
    http://www.thefreelibrary.com/.....a014909330

    Or better yet DrREC, if you want to actually ‘prove’ that neo-Darwinism actually has a proper place at the table of modern science, then simply falsify Alain Aspects falsification of local realism (materialism) so that you may be able to explain the quantum entanglement found in DNA and proteins by materialistic (neo-Darwinian) means!!! Until then, everything you do is mere ‘rationalization’ parading as science!!

    2 Peter 1:16
    ‘For we have not followed cunningly devised fables,’

  43. BA77:

    “The protein machine clearly demonstrates ‘teleology’ in its design. Teleological Design which requires the foresight of a designer to choose the correct path out of a nearly infinite number of incorrect paths;”

    I don’t understand. If the mechanism was built up based on a trial-and-error system of saving what works and throwing away what doesn’t work how is that teleological?

    Back later, just getting dinner ready.

  44. Upright: No one said they just happened to be floating by at just the right time!!

    I know you get frustrated that people misrepresent ID. Please don’t misrepresent evolution. It gets us no where.

  45. Ellazimm you state;

    ‘I don’t understand. If the mechanism was built up based on a trial-and-error system of saving what works and throwing away what doesn’t work how is that teleological?’

    So you believe that blind neo-Darwinian processes have built a ‘novel protein making machine’ that automatically knows where all the functional proteins are in sequence space??? Two problems I can think of right off the bat;

    One problem is this:

    “There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system only a variety of wishful speculations. It is remarkable that Darwinism is accepted as a satisfactory explanation of such a vast subject.”
    James Shapiro – Molecular Biologist

    The following expert doesn’t even hide his very unscientific preconceived philosophical bias against intelligent design,,,

    ‘We should reject, as a matter of principle, the substitution of intelligent design for the dialogue of chance and necessity,,,

    Yet at the same time the same expert readily admits that neo-Darwinism has ZERO evidence for the chance and necessity of material processes producing any cellular system whatsoever,,,

    ,,,we must concede that there are presently no detailed Darwinian accounts of the evolution of any biochemical or cellular system, only a variety of wishful speculations.’
    Franklin M. Harold,* 2001. The way of the cell: molecules, organisms and the order of life, Oxford University Press, New York, p. 205.
    *Professor Emeritus of Biochemistry, Colorado State University, USA

    Michael Behe – No Scientific Literature For Evolution of Any Irreducibly Complex Molecular Machines
    http://www.metacafe.com/watch/5302950/

    “The response I have received from repeating Behe’s claim about the evolutionary literature, which simply brings out the point being made implicitly by many others, such as Chris Dutton and so on, is that I obviously have not read the right books. There are, I am sure, evolutionists who have described how the transitions in question could have occurred.” And he continues, “When I ask in which books I can find these discussions, however, I either get no answer or else some titles that, upon examination, do not, in fact, contain the promised accounts. That such accounts exist seems to be something that is widely known, but I have yet to encounter anyone who knows where they exist.”
    David Ray Griffin – retired professor of philosophy of religion and theology

    Another problem you have ellazimm for your imaginary ‘virtually error free novel protein making machine’ is that the information/knowledge that the protein making machine would have to have access to, for determining which proper protein to use for any specific situation, approaches infinity;

    Francis Collins on Making Life
    Excerpt: ‘We are so woefully ignorant about how biology really works. We still don’t understand how a particular DNA sequence—when we just stare at it—codes for a protein that has a particular function. We can’t even figure out how that protein would fold—into what kind of three-dimensional shape. And I would defy anybody who is going to tell me that they could, from first principles, predict not only the shape of the protein but also what it does.’ – Francis Collins – Former Director of the Human Genome Project

    In the year 2000 IBM announced the development of a new super-computer, called Blue Gene, which was 500 times faster than any supercomputer built up until that time. It took 4-5 years to build. Blue Gene stands about six feet high, and occupies a floor space of 40 feet by 40 feet. It cost $100 million to build. It was built specifically to better enable computer simulations of molecular biology. The computer performs one quadrillion (one million billion) computations per second. Despite its speed, it was estimated to take one entire year for it to analyze the mechanism by which JUST ONE “simple” protein will fold onto itself from its one-dimensional starting point to its final three-dimensional shape.

    “Blue Gene’s final product, due in four or five years, will be able to “fold” a protein made of 300 amino acids, but that job will take an entire year of full-time computing.” Paul Horn, senior vice president of IBM research, September 21, 2000
    http://www.news.com/2100-1001-233954.html

    Networking a few hundred thousand computers together has reduced the time to a few weeks for simulating the folding of a single protein molecule:

    A Few Hundred Thousand Computers vs. A Single Protein Molecule – video
    http://www.metacafe.com/watch/4018233

    As well, despite some very optimistic claims, it seems future ‘quantum computers’ will not fair much better in finding functional proteins in sequence space than even a idealized ‘material’ supercomputer of today can do:

    The Limits of Quantum Computers – March 2008
    Excerpt: “Quantum computers would be exceptionally fast at a few specific tasks, but it appears that for most problems they would outclass today’s computers only modestly. This realization may lead to a new fundamental physical principle”
    http://www.scientificamerican......-computers

    The Limits of Quantum Computers – Scott Aaronson – 2007
    Excerpt: In the popular imagination, quantum computers would be almost magical devices, able to “solve impossible problems in an instant” by trying exponentially many solutions in parallel. In this talk, I’ll describe four results in quantum computing theory that directly challenge this view.,,, Second I’ll show that in the “black box” or “oracle” model that we know how to analyze, quantum computers could not solve NP-complete problems in polynomial time, even with the help of nonuniform “quantum advice states”,,,
    http://www.springerlink.com/co.....330115207/

    Here is Scott Aaronson’s blog in which refutes recent claims that P=NP (Of note: if P were found to equal NP, then a million dollar prize would be awarded to the mathematician who provided the proof that NP problems could be solved in polynomial time):

    Shtetl-Optimized
    Excerpt: Quantum computers are not known to be able to solve NP-complete problems in polynomial time.
    http://scottaaronson.com/blog/?p=456

    Protein folding is found to be a ‘intractable NP-complete problem’ by several different methods. Thus protein folding will not be able to take advantage of any advances in speed that quantum computation may offer to any other problems of computation that may be solved in polynomial time:

    Combinatorial Algorithms for Protein Folding in Lattice
    Models: A Survey of Mathematical Results – 2009
    Excerpt: Protein Folding: Computational Complexity
    4.1
    NP-completeness: from 10^300 to 2 Amino Acid Types
    4.2
    NP-completeness: Protein Folding in Ad-Hoc Models
    4.3
    NP-completeness: Protein Folding in the HP-Model
    http://www.cs.brown.edu/~sorin.....survey.pdf

    etc.. etc… etc…

  46. 46

    Hello again, Ellazimm

    I have no need to misrepresent evolution. However, when someone explains away magnitudes of organization by appeal to the notion that it all works together just fine – then I react.

    The comment above has been made so many times it is beyond count. We are material organisms living in a material universe – of course its going to work together. That does not mean that everything in action in the universe can be reduced to material causes. To get to that partiocular conclusion, one must begin by making an assumption that the conclusion is true, then steadfastly refusing to test it.

  47. 47

    By the way Ellaziim,

    I am glad you’ve stuck around. I have enjoyed reading your exchanges with KF and others. As opponents go, you’re starting to grow on me. :)

    Cheers

  48. Upright: Thank you, I am trying to be civil and respectful but still ask questions. I’m just finishing up with my family for the evening and I’m going to do my best to get back to you and your comment and BA77. I’m sorry I’ve not got more time or expertise though. I’d much rather hand over things to someone else!!

    ~part of the loyal opposition

  49. DrREC, back to this peculiar statement of your;

    ‘Both genomes are sequenced. You can do the BLAST searches yourself.’

    So?? My whole point is that you cannot extrapolate genetic similarity to conclusive scientific proof that neo-Darwinian evolution produced the changes!! To maintain scientific legitimacy, you must actually demonstrate that purely material, neo-Darwinian, processes can accomplish all that you ascribe to them. Just because you, and a horde of triple PHDs., believe it to be possible, does not impress me in the least!!! Like I said, if you want to impress me, change one bacterium into another species of bacterium, or if that is to hard for you, and your horde of triple PhDs, perhaps you can pass this simple fitness test;

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    Something tells me that even this extremely simple test is too much for you, and your horde, and that you will simply ignore this crucial test that you must pass to stay scientifically legitimate, simply because it does not fit your ‘religion’ of neo-Darwinian evolution:

    Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009
    Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own.
    http://www.discovery.org/a/9951

    Michael Behe’s Quarterly Review of Biology Paper Critiques Richard Lenski’s E. Coli Evolution Experiments – December 2010
    Excerpt: After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs)
    http://www.evolutionnews.org/2.....41221.html

    Testing Evolution in the Lab With Biologic Institute’s Ann Gauger – podcast with link to peer-reviewed paper
    Excerpt: Dr. Gauger experimentally tested two-step adaptive paths that should have been within easy reach for bacterial populations. Listen in and learn what Dr. Gauger was surprised to find as she discusses the implications of these experiments for Darwinian evolution. Dr. Gauger’s paper, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,”.
    http://intelligentdesign.podom.....4_13-07_00

    ,,,,But as to this statement of yours once again;

    ‘Both genomes are sequenced. You can do the BLAST searches yourself.’

    Well DrREC, just what kind of consistency do we find if different people look at the sequences???:

    Chimpanzee?
    10-10-2008 – Dr Richard Buggs – research geneticist at the University of Florida
    …Therefore the total similarity of the genomes could be below 70%.
    http://www.idnet.com.au/files/pdf/Chimpanzee.pdf

    A simple statistical test for the alleged “99% genetic identity” between humans and chimps – September 2010
    Excerpt: The results obtained are statistically valid. The same test was previously run on a sampling of 1,000 random 30-base patterns and the percentages obtained were almost identical with those obtained in the final test, with 10,000 random 30-base patterns. When human and chimp genomes are compared, the X chromosome is the one showing the highest degree of 30BPM similarity (72.37%), while the Y chromosome shows the lowest degree of 30BPM similarity (30.29%). On average the overall 30BPM similarity, when all chromosomes are taken into consideration, is approximately 62%.
    http://www.uncommondescent.com.....nd-chimps/

    Do Human and Chimpanzee DNA Indicate an Evolutionary Relationship?
    Excerpt: the authors found that only 48.6% of the whole human genome matched chimpanzee nucleotide sequences. [Only 4.8% of the human Y chromosome could be matched to chimpanzee sequences.]
    http://www.apologeticspress.org/articles/2070

    DNA Comparisons between Humans and Chimps – Fazale Rana
    Excerpt: It is interesting that when evolutionary biologists discuss genetic comparisons between human and chimpanzee genomes, the fact that, again, as much as 25 percent of the two genomes won’t align receives no mention. Instead, the focus is only on the portions of the genome that display a high-degree of similarity. This distorted emphasis makes the case for the evolutionary connection between humans and chimps seem more compelling than it may actually be.
    http://www.reasons.org/dna-com.....del-part-2

    But of course this will matter not one iota to you DrREC because??? because??? well because by-golly fudging genetic similarity is the only thing you got that can make it seem to the unsuspecting public that you got evidence for neo-Darwinian evolution!!!

  50. Upright: I never thought I would be able to make any kind of argument you haven’t heard before. I do not expect to change anyone’s mind. Which is fine. If i wanted to change your mind I’d pick a different approach. I really am just trying to understand how you see and interpret the evidence. Really. I shouldn’t really even spend time defending my view but I don’t like to turn down a request.

    So no, I haven’t got much to add to the statements you’ve heard before. Sorry.

    BA77: You know the arguments for rejecting design as a possible explanation and I’m not here to defend those arguments. I am here to find out why you think design IS a valid assumption. And you’ve been giving me lots of good info for that.

    You say: “Another problem you have ellazimm for your imaginary ‘virtually error free novel protein making machine’ is that the information/knowledge that the protein making machine would have to have access to, for determining which proper protein to use for any specific situation, approaches infinity;”

    Well, I don’t think there is a virtual error free novel protein making machine. I think the history of evolution is littered with mistakes and errors. It’s a messy and wasteful process. Most species that ever lived are now extinct. Good for our petroleum reserves but non-sensical from a design point of view IN MY OPINION.

    Francis Collins is being frank and honest: there’s a lot we don’t know. But the general trend seems very clear.

    I agree the protein folding problem is complex. Very complex. Maybe even NP-complete. But remember the definition of NP-complete. A decision problem L is NP-complete if it is in the set of NP problems so that any given solution to the decision problem can be verified in polynomial time, and also in the set of NP-hard problems so that any NP problem can be converted into L by a transformation of the inputs in polynomial time.

    That doesn’t mean that there isn’t an ‘optimal’ solution. Or that brute force methods won’t work. And evolution is, in my view, a brute force method, sort of. I say sort of because biological systems that are at all viable are given their time in the sun even if they’re NOT optimal.

    I don’t understand the discussion of NP-complete here. It may be true that finding protein folding is analogous to the travelling salesman problem but even the travelling salesman problem can be solved with brute force. And,it’s seldom, in a biological system, that only the optimal solution is viable. In fact, this is part of the point of evolution: if it plays it stays. Even if it’s NOT the best or greatest.

    It reminds me of kairofocus’s discussion of having to search the whole solution space. Why? If something comes up that’s okay it does its best to survive. Only mathematicians search for the optimal solution. Biologists, engineers, computer programmers . . . they all make things good enough. Ask Gil. I bet he’s never written a chunk of code that he thought was optimal, the best it could be. I’d bet that every single deliverable he’s made he wishes he had more time to polish.

    Speaking of which . . . (sorry for putting it here) I was thinking about the DNA like computer code paradigm.

    Most computer code follows general formats common to lots of code: there’s an introduction usually composed of variable declerations and function and procedure definitions. Then there’s the body of the algorithm.

    I’m not saying DNA should follow THAT outline but if it’s designed then wouldn’t it be fair to look for some kind of common format? I think so.

    But then we’d have to look at why so many different species’ genomes have widely different number of base pairs and genes and chromosomes.

    But what do you think?

  51. Sorry, i’m writing way more than I really want to. I hate being boring.

  52. BA77: I know YOU accept the interpretations made in lots of your links; I consider you to be a sincere, caring, empathetic individual. But it doesn’t mean that the views of Drs Dembski, Behe, Meyrs, Wells, etc are accepted or even correct.

    At the very least you need to consider all the evidence including that which you find dismissive of your paradigm. I’m here to do that very thing, to find out what you see as support for your views. And, I have to say, reading through the Lynn Margulis interview you referenced was a real eye-openier for me. I’ve thought about it all day. And she said that some of your criticisms of the consensus view of evolution are correct!

    I just ask that you show a modicum of respect for views different from your own. Which is what I’m trying to de.

  53. 53

    Hi Ellazimm,

    I am not asking you to change your mind either. The conversations that take place here are for the gallery who wish to view the discussion on their own terms. The purpose of my comment above was merely to point out that appealling to the fact that material objects act materially is well – silly, quite frankly.

    No ID arguments suggests otherwise.

  54. Upright-let me clarify my statement regarding BA77′s post:

    “How does the protein machine at the end of the preceding video (Chaperone) know exactly how to fold each unique protein into its proper, and unique, structure??? That machine, by itself, clearly displays ‘foresight and planning”

    I replied:
    “Chaperones tend to have high affinity for the extended and hydrophobic bits of an unfolded protein, and less affinity for the compact, folded bit. No foresight and imagination-just physical properties of protein folding.”

    The no foresight and imagination refers to the current functioning of a chaperone-which is mechanistic. No computer attached, no brain.

    I made no comment on the origin of the chaperone machinery-and there is a world of difference between materialist functioning (and machine) and materialist origins.

    I don’t particularly think it is possible or scientific to demonstrate chaperones lack telic origins.

    I might refer back to Cornelius Hunter’s discussions on de novo genes-that even if a strictly material pathway for the evolution of some protein is found, it does not rule out that that process was not influenced by a non-material force.

    We thus return to sentiments echoed here (which sound like theistic evolution to me):

    http://www.uncommondescent.com.....-biologos/

  55. Bornagain77-really, you’ve got to slow down. You’re posting things we’ve already discussed-like the non-aligned portion of the Chimp genome, which is due to ambiguous alignments of repetitive bits and is way down from the 25% in the first draft!

    I really don’t want to go in circles on these, but I couldn’t help myself on this one:

    “Just because you, and a horde of triple PHDs.”

    I don’t personally know anyone with more than one Ph.D.

    “Like I said, if you want to impress me, change one bacterium into another species of bacterium, or if that is to hard for you, and your horde of triple PhDs, ”

    Bacteria:

    Mutation, recombination, and incipient speciation of bacteria in the laboratory
    http://www.pnas.org/content/96/13/7348.full.pdf

    Yeast:

    Incipient speciation by divergent adaptation and antagonistic epistasis in yeast
    http://www.nature.com/nature/j.....05856.html

    Worms:

    Weinberg, J. R., V. R. Starczak and P. Jora. 1992. Evidence for rapid speciation following a founder event in the laboratory. Evolution. 46:1214-1220.

    Flies (among many papers)….

    Schluter, D. and L. M. Nagel. 1995. Parallel speciation by natural selection. American Naturalist. 146:292-301.

    Plants-created a whole genus-Raphanobrassica

    Karpechenko, G.D., Polyploid hybrids of Raphanus sativus L. X Brassica oleracea L. Zeitschrift für induktive Abstammungs- und Vererbungslehre 48, 1–85 (1928)

  56. 56

    Dr,

    My comment was quite obviously an adjunct to yours, and was intended to neither challenge nor misrepresent your position in any way. I only wished to highlight the triviality of suggesting that material things operate materially. The world is full of objects that act purely in the material realm, but cannot be accounted for by purely material causes – unless you simply assume materialism from the outset. A red plastic ball is a perfect example.

    cheers…

  57. DrREC you state:

    ‘the non-aligned portion of the Chimp genome, which is due to ambiguous alignments of repetitive bits and is way down from the 25% in the first draft!’

    Only if you take neo-Darwinian presupposition as true!!!. Remember you are the one who said I can look at the sequences myself. And when the sequences are looked at with ‘non-Darwinian’ glasses, your whole argument falls apart!!! But how did I know that any interpretation except a neo-Darwinian interpretation would not be accepted by you!!!

    then;

    Bacteria: ‘incipient speciation’

    yet;

    in·cip·i·ent/in?sip??nt/Adjective
    1. In an initial stage; beginning to happen or develop:

    and,,

    from what I can tell all the adaptations of the bacteria were well within ‘Genetic Entropy’, Moreover Lenski’s name was on the paper, and his subsequent work on e-coli, which exceeds this ‘dated 1999′ paper, that you cited, reveals quite a lot actually, A lot that undermines neo-Darwinism;

    These following articles refute Richard E. Lenski’s ‘supposed evolution’ of the citrate ability for the E-Coli bacteria after 20,000 generations of the E-Coli from his ‘Long Term Evolution Experiment’ (LTEE) which has been going on since 1988:

    Multiple Mutations Needed for E. Coli – Michael Behe
    Excerpt: As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.” (1) Other workers (cited by Lenski) in the past several decades have also identified mutant E. coli that could use citrate as a food source. In one instance the mutation wasn’t tracked down. (2) In another instance a protein coded by a gene called citT, which normally transports citrate in the absence of oxygen, was overexpressed. (3) The overexpressed protein allowed E. coli to grow on citrate in the presence of oxygen. It seems likely that Lenski’s mutant will turn out to be either this gene or another of the bacterium’s citrate-using genes, tweaked a bit to allow it to transport citrate in the presence of oxygen. (He hasn’t yet tracked down the mutation.),,, If Lenski’s results are about the best we’ve seen evolution do, then there’s no reason to believe evolution could produce many of the complex biological features we see in the cell.
    http://behe.uncommondescent.co.....or-e-coli/

    Michael Behe’s Quarterly Review of Biology Paper Critiques Richard Lenski’s E. Coli Evolution Experiments – December 2010
    Excerpt: After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs)
    http://www.evolutionnews.org/2.....41221.html

    Lenski’s e-coli – Analysis of Genetic Entropy
    Excerpt: Mutants of E. coli obtained after 20,000 generations at 37°C were less “fit” than the wild-type strain when cultivated at either 20°C or 42°C. Other E. coli mutants obtained after 20,000 generations in medium where glucose was their sole catabolite tended to lose the ability to catabolize other carbohydrates. Such a reduction can be beneficially selected only as long as the organism remains in that constant environment. Ultimately, the genetic effect of these mutations is a loss of a function useful for one type of environment as a trade-off for adaptation to a different environment.
    http://www.answersingenesis.or.....n-bacteria

    Lenski’s work actually did do something useful in that it proved that ‘convergent evolution’ is impossible because it showed that evolution is ‘historically contingent’. This following video and article make this point clear:

    Lenski’s Citrate E-Coli – Disproof of Convergent Evolution – Fazale Rana – video (the disproof of convergence starts at the 2:45 minute mark of the video)
    http://www.metacafe.com/watch/4564682

    The Long Term Evolution Experiment – Analysis
    Excerpt: The experiment just goes to show that even with historical contingency and extreme selection pressure, the probability of random mutations causing even a tiny evolutionary improvement in digestion is, in the words of the researchers who did the experiment, “extremely low.” Therefore, it can’t be the explanation for the origin and varieity of all the forms of life on Earth.
    http://www.scienceagainstevolution.org/v12i11f.htm

    The loss of ‘convergent evolution’, as a argument for molecular sequence similarity, is a major blow to neo-Darwinian story telling:

    Implications of Genetic Convergent Evolution for Common Descent – Casey Luskin – Sept. 2010
    Excerpt: When building evolutionary trees, evolutionists assume that functional genetic similarity is the result of inheritance from a common ancestor. Except for when it isn’t. And when the data doesn’t fit their assumptions, evolutionists explain it away as the result of “convergence.” Using this methodology, one can explain virtually any dataset. Is there a way to falsify common descent, even in the face of convergent genetic similarity? If convergent genetic evolution is common, how does one know if their tree is based upon homologous sequences or convergent ones? Critics like me see the logic underlying evolutionary trees to be methodologically inconsistent, unpersuasive, and ultimately arbitrary.
    http://www.evolutionnews.org/2.....37841.html

    You then cite a yeast paper with that ‘incipient’ ‘beginning to’ word in it again,,,!!!

    Then you dig way back to 1992 for this;

    ‘Evidence for rapid speciation following a founder event in the laboratory’

    So what??? Rapid SUB-speciation is actually a argument against neo-Darwinism:

    ,,,Evidence for rapid radiations of a sub-species from a parent species can be found here:

    Biological Variation – Cornelius Hunter
    Excerpt: One hint that biology would not cooperate with Darwin’s theory came from the many examples of rapidly adapting populations. What evolutionists thought would require thousands or millions of years has been observed in laboratories and in the field, in an evolutionary blink of an eye.
    http://www.darwinspredictions......_variation

    These following studies and video, on Cichlid fishes, are evidence of the ‘limited and rapid variation from a parent kind’ predicted by the Genetic Entropy model:

    African cichlid fish: a model system in adaptive radiation research:
    “The African cichlid fish radiations are the most diverse extant animal radiations and provide a unique system to test predictions of speciation and adaptive radiation theory(of evolution).—-surprising implication of the study?—- the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages”

    HMMM, parent species always radiate more rapidly than sub-species???? Which theory predicts that as a starting presupposition DrREC???

    Multiple Genes Permit Closely Related Fish Species To Mix And Match Their Color Vision – Oct. 2005
    Excerpt: In the new work, the researchers performed physiological and molecular genetic analyses of color vision in cichlid fish from Lake Malawi and demonstrated that differences in color vision between closely related species arise from individual species’ using different subsets of distinct visual pigments.

    Cichlid Fish – Evolution or Variation Within Kind? – Dr. Arthur Jones – video
    http://www.metacafe.com/watch/4036852

    Materialists may have trouble explaining such evidence for ‘robust and rapidly adapting genomes’ from ancient parent lineages, but Genetic Entropy holds ancient parent lineages will always have a more robust genome than their sub-species.

    etc.. etc.. etc..

    “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)-but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.”
    R. Milner, Encyclopedia of Evolution (1990)

    Poly-Functional Complexity equals Poly-Constrained Complexity
    https://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjdoZmd2emZncQ

  58. ellazimm: “Biologists, engineers, computer programmers . . . they all make things good enough. Ask Gil. I bet he’s never written a chunk of code that he thought was optimal, the best it could be. I’d bet that every single deliverable he’s made he wishes he had more time to polish.”

    Precisely. Which is why the suboptimal (or sometimes called “poor design”) argument against ID is invalid.

    Yet even with Gil’s suboptimal program, there is an overarching structure, something that makes it hang together, some fundamental amount of information content and functionality that, in our experience, only comes from planned, purposeful activity.

    One can, of course, imagine that such integrated, functional complexity can arise through a long series of accidents, but it is a pretty tough row to hoe, from a logical standpoint.

    I’m talking about an overarching principle here, not disputing a particular instance of base-pair mutations, insertions, deletions, or even species-species relatedness.

  59. Eric: Well, I’ll let you speculate on sub-optimal design! I’m done with guessing about the ability or goals of the designer(s). :-)

    As far as an overarching structure is concerned I would think that is worth looking at. What I cannot figure out is why the size of the genome should vary so greatly. For instance pieris japonica’s genome has 150 billion base pairs where as the human genome has 3.2 billion. The disparity is fascinating. Or what about tetraodon nigroviridis (type of puffer fish) which has a genome of only 385 million base pairs whereas protopterus aethiopicus (marbled lungfish) has 130 billion base pairs? Does a lungfish really have several orders of magnitude more information in its genome? Is the code structured that much differently, less efficiently? Fascinating.

    BA77: Can you give me a comprehensive definition of kind? One of your references brought that up and I must admit I’ve never really gotten my head around it. Which taxonomic category is it equivalent too? Have you got a list of kinds?

  60. Ellazimm you state;

    ‘Does a lungfish really have several orders of magnitude more information in its genome? Is the code structured that much differently, less efficiently?’

    So??? Do you want to argue theology or science? At the base of your argument you are presupposing that you can design a organism better than God! i.e. God would not have done that way, therefore materialistic neo-Darwinism must be true! How very humble of you. NOT! ellazimm once again I remind you that you are using your theology to try to prove your scientific presupposition, instead of using science to try to prove your theological presupposition!!! This is completely backwards! You are completely blind to the fact that you cannot even show me one functional protein that was arrived at by purely materialistic processes!!! Nor can you using all you intelligence, or unguided materialistic processes in particular, even come close to generating the unmatched levels of programming we find in genomes!! Thus, Why don’t you address your science on its merits instead of using theologically based arguments to try to prove your point? Like I said, do you want to argue science or Theology???

    as to your second question:

    Can you give me a comprehensive definition of kind?

    A review of The Edge of Evolution: The Search for the Limits of Darwinism by Michael J. Behe
    Excerpt: So Michael Behe comes to the grand conclusion to his survey: ‘Somewhere between the level of vertebrate species and class lies the organismal edge of Darwinian evolution’ (p. 201). A diagram illustrates this (p. 218), which he reproduces on the page facing the title page of the book (figure 2).

    Interestingly, the creationist study of baraminology (defining the limits of the original created kinds, or baramins, of Genesis 1) has arrived at conclusions consistent with Behe’s proposition, using a different approach based on hybridization criteria, where possible, combined with morphology, etc.4 In fact, in 1976 creationist biologist Frank Marsh proposed that the created kinds (baramins) were often at the level of genus or family, although sometimes at the level of order.5
    http://creation.com/review-mic.....-evolution

  61. Has anyone ever done a complete side by side comparison of a human and chimp genome?

    And if not does anyone know what they are waiting for?

    Or do they not care what the real % difference is?

  62. BA77: Thanks for the link regarding baraminology; I’ll have a look.

    I didn’t think I was trying to prove a point about the sizes of different genomes, I was just asking a question.

    From a design point of view what reasons would there be to have such huge disparities in the number of base pairs? I tossed in a couple of possibilities.

    If that’s an inappropriate question then tell me why. I certainly do not think I can do a better job.

  63. Joseph, This site may interest you:

    Do Human and Chimpanzee DNA Indicate an Evolutionary Relationship?
    by Bert Thompson, Ph.D.
    Brad Harrub, Ph.D.

    REAL GENOMIC DIFFERENCES

    One of the downfalls of previous molecular genetic studies has been the limit at which chimpanzees and humans could be compared accurately. Scientists often would use only 30 or 40 known proteins or nucleic acid sequences, and then from those extrapolate their results for the entire genome. Today, however, we have the majority of the human genome sequences, practically all of which have been released and made public. This allows scientists to compare every single nucleotide base pair between humans and primates—something that was not possible prior to the human genome project. In January 2002, a study was published in which scientists had constructed and analyzed a first-generation human chimpanzee comparative genomic map. This study compared the alignments of 77,461 chimpanzee bacterial artificial chromosome (BAC) end sequences to human genomic sequences. Fujiyama and colleagues “detected candidate positions, including two clusters on human chromosome 21, that suggest large, nonrandom regions of differences between the two genomes” (2002, 295:131). In other words, the comparison revealed some “large” differences between the genomes of chimps and humans.

    Amazingly, the authors found that only 48.6% of the whole human genome matched chimpanzee nucleotide sequences. [Only 4.8% of the human Y chromosome could be matched to chimpanzee sequences.] This study compared the alignments of 77,461 chimpanzee sequences to human genomic sequences obtained from public databases. Of these, 36,940 end sequences were unable to be mapped to the human genome (295:131). Almost 15,000 of those sequences that did not match human sequences were speculated to “correspond to unsequenced human regions or are from chimpanzee regions that have diverged substantially from humans or did not match for other unknown reasons” (295:132). While the authors noted that the quality and usefulness of the map should “increasingly improve as the finishing of the human genome sequence proceeds” (295:134), the data already support what creationists have said for years—the 98-99% figure representing DNA similarity is grossly misleading, as revealed in a study carried out by Roy Britten of the California Institute of Technology (see Britten, 2002).
    http://www.apologeticspress.or.....ticle=1038

  64. BA77: From the review of The Edge of Evolution you linked to:

    “And then it gets really confusing. Behe says that science has revealed a fine tuning ‘well beyond laws, past details, into the very fabric of life’ (p. 230). ‘But the assumption that design unavoidably requires “interference” rests mostly on a lack of imagination. There’s no reason that the extended fine-tuning view I am presenting here necessarily requires active meddling with nature any more than the fine-tuning of theistic evolution does. One can think the universe is finely tuned to any degree and still conceive that “the universe originated by a single creative act” and underwent “its natural development by laws implanted in it.” One simply has to envision that the agent who caused the universe was able to specify from the start not only laws but much more.’”

    And later:

    “Behe also seems confused about common descent, which he repeatedly asserts that he accepts. He accepts the evolutionists’ argument that shared supposed DNA errors demonstrate common descent (that humans and chimps had a common ancestor, for example). But the argument depends on the assumption that so-called ‘pseudogenes’ are functionless. Behe himself inadvertently provides the evidence against the idea, in discussing the prevalence of mutations (p. 68). If we assume the evolutionary scenario of millions years since our split from a common ancestor with chimps, if the ‘pseudogene’ were functionless, unconstrained by natural selection, then it should have mutated almost beyond recognition. But it hasn’t—the close similarity is claimed as evidence of common ancestry! So, using the evolutionists’ own assumptions, it is not ‘useless’ and the evolutionary argument disintegrates and the similarity becomes evidence for common design, not common ancestry.”

    But . . . if no further ‘active meddling. took place then how did all the ‘kinds’ arise later? Am I just missing something?

    It would be interesting to see a full layout of all the kinds; is there such a table/graphic?

  65. ellazimm, you ask;

    ‘From a design point of view what reasons would there be to have such huge disparities in the number of base pairs?’

    There are a number of reasons for why it could be that way, but we are not at that point yet of ‘speculation’ for you must first answer this question conclusively to have a case to build on.
    Is or is not design present in the genome? If not then please present your scientific evidence that purely material processes can generate any functional information whatsoever!

    notes:

    The Law of Physicodynamic Insufficiency – Dr David L. Abel – November 2010
    Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.”
    http://www.scitopics.com/The_L.....iency.html

    ellazimm; Dr. Craig exposed Ayala, in this following video, for trying to use the style of argumentation you are trying to use now:

    Refuting The “Bad Design” Vs. Intelligent Design Argument – William Lane Craig – video
    http://www.metacafe.com/watch/4109211/

    This recent peer reviewed article exposed the fact that Darwin’s book, Origin of Species, is actually, first and foremost, a Theological book trying to establish a scientific fact;

    Charles Darwin, Theologian: Major New Article on Darwin’s Use of Theology in the Origin of Species – May 2011
    Excerpt: Dilley argues, Darwin employed theology in a positive fashion, as support for his own position. “In the Origin,” Dilley writes, “Darwin used a specific theological view of God’s relationship to natural laws in order to argue for evolution and against special creation.” The Origin supplies abundant evidence of theology in action; as Dilley observes:

    I have argued that, in the first edition of the Origin, Darwin drew upon at least the following positiva theological claims in his case for descent with modification (and against special creation):

    1. Human begins are not justfied in believing that God creates in ways analogous to the intellectual powers of the human mind.

    2. A God who is free to create as He wishes would create new biological limbs de novo rather than from a common pattern.

    3. A respectable deity would create biological structures in accord with a human conception of the ‘simplest mode’ to accomplish the functions of these structures.

    4. God would only create the minimum structure required for a given part’s function.

    5. God does not provide false empirical information about the origins of organisms.

    6. God impressed the laws of nature on matter.

    7. God directly created the first ‘primordial’ life.

    8. God did not perform miracles within organic history subsequent to the creation of the first life.

    9. A ‘distant’ God is not morally culpable for natural pain and suffering.

    10. The God of special creation, who allegedly performed miracles in organic history, is not plausible given the presence of natural pain and suffering.
    http://www.evolutionnews.org/2.....46391.html

    further notes:

    Science Owes Nothing To Darwinian Evolution – Jonathan Wells – video
    http://www.metacafe.com/watch/4028096

    “Certainly, my own research with antibiotics during World War II received no guidance from insights provided by Darwinian evolution. Nor did Alexander Fleming’s discovery of bacterial inhibition by penicillin. I recently asked more than 70 eminent researchers if they would have done their work differently if they had thought Darwin’s theory was wrong. The responses were all the same: No.
    Philip S. Skell – Professor at Pennsylvania State University.
    http://www.discovery.org/a/2816

    Podcasts and Article of Dr. Skell
    http://www.evolutionnews.org/2.....40981.html

  66. BA77: I don’t understand how the proposed failings of mechanical processes to create major morphological body features affect the appropriateness of asking how design theory explains the incredible variety of genome sizes. I am not saying it’s bad design. I’m asking you what you think!

    If you’re waiting for me to capitulate I’m sorry but I’m not here to defend or reject common descent with modification (and gene stealing?). As I’ve said before. I’m hear to learn how design theory ‘works’ and how it accounts for some of the data.

  67. ellazimm you state;

    ‘It would be interesting to see a full layout of all the kinds; is there such a table/graphic?’

    Sure, go to almost any comprehensive fossil graph, remove all the dotted lines that indicate ‘hypothesized’ evolutionary transitions, for which they have no evidence, and there you have you graph.

    notes:

    Here are some VERY coarse outlines of the fossil record:

    Origin of Phyla – The Fossil Evidence – Timeline Graph
    http://docs.google.com/Doc?doc.....#038;hl=en

    Here is a graph showing a partial list of fossil groups showing their sudden appearance in the fossil record- (without the artificially imposed dotted lines) – Timeline Illustration:
    http://www.earthhistory.org.uk.....groups.jpg

    The Truth About Evolution – Transitional Fossils
    Excerpt: Major adaptive radiations provide a formidable challenge to biological evolution.,,, Major adaptive radiations of groups of vertebrates are:

    a) Placoderms in the early Devonian. Because they were heavily armored, jawed fish, intermediates and ancestral forms should have fossilized but none are found. No placoderms exist today.
    b) Chondrichtyes during the Devonian. They are the cartilaginous fish such as sharks and rays. Intermediates and ancestors are unknown.
    c) Agnatha Fish in the Silurian. These were jawless fish with bony skeletons. Intermediates and ancestors should have fossilized but none are found. Most types became extinct but hagfish and lampreys are living jawless fish.
    d)Tetrapods in the early Carboniferous. These were many, diverse forms of four-legged amphibians that are believed to have evolved from fish. But no fossilized links to fish have been found and specific interrelationships of the numerous lineages is unknown.
    e) Amniotes in the late Carboniferous. Amniotes are characterized by their complex reproductive system and include reptiles, birds and mammals. They are believed to have evolved from amphibians but their ancestry has not been determined from the fossil record.
    f) Archosaurs in the late Permian. They were reptiles with diverse sizes and shapes that became extinct in the Triassic. Some as long as six meters have been found.
    g ) Dinosaurs in the late Triassic. Dinosaurs include the largest terrestrial animals that have ever lived. Their diversity in size and shape was spectacular. Their ancestry is unknown and specific interrelationships of the numerous types is unknown.
    h) Teleosts in the late Cretaceous. These are bony fish approximately 20,000 living species in 35 orders and 409 families. Interrelationships of the higher groups are unknown.
    i) Therian mammals in the late Cretaceous and early Tertiary. These are placental and marsupial mammals. When they first appear in the fossil record, they are very diverse and interrelationships are unknown.
    j) Birds in the late Cretaceous and early Tertiary. There are estimates of 8900 living species in 166 families and about 27 orders. Fossil evidence is lacking for establishing the interrelationships of the orders of birds.
    http://tellall.org/fossils.htm

    “The history of most fossil species includes two features inconsistent with gradualism:. Statis. Most species exhibit no directional change during their tenure on earth. They appear in the fossil record looking much the same as when they disappear…. Sudden Appearance. In any local area, a species does not arise gradually by the steady transformation of its ancestors; it appears all at once and ‘fully formed’. The evolutionary trees that adorn our textbooks have data only at the tips and nodes of their branches; the rest is inference, however reasonable, not the evidence of fossils.”
    Stephen Jay Gould, – Evolution’s Erratic Pace – 1977

    “Many species remain virtually unchanged for millions of years, then suddenly disappear to be replaced by a quite different, but related, form. Moreover, most major groups of animals appear abruptly in the fossil record, fully formed, and with no fossils yet discovered that form a transition from their parent group.”
    (C.P. Hickman, L.S. Roberts, and F.M. Hickman, Integrated Principles of Zoology, p. 866 (1988, 8th ed.).
    http://www.evolutionnews.org/2.....39831.html

    The Fossil Record – The Evolutionary Myth Of +99% Extinct Species – Dr. Arthur Jones – video
    http://www.metacafe.com/watch/4028115/

    “Why, if species have descended from other species by fine gradations, do we not everywhere see innumerable transitional forms? Why is not all nature in confusion, instead of the species being, as we see them, well defined? But, as by this theory innumerable transitional forms must have existed, why do we not find them embedded in countless numbers in the crust of the earth? But in the intermediate region, having intermediate conditions of life, why do we not now find closely-linking intermediate varieties?”
    Charles Darwin – Origin Of Species

  68. ellazimm per 66, you refuse to defend your position, yet have the audacity to use the ‘bad design argument’??? Sorry I ain’t going to play your game!!~ Basically what you are telling me is, “well yeah, I can’t produce any evidence for material processes generating functional information, but none-the-less, despite having no foundation in science, I reserve the right to argue theodicy for neo-Darwinism.

  69. BA77: I’m not using an argument at all! I’m asking a question! And I didn’t think I was arguing theodicy. And you already know all the standard defences of my position, me repeating them doesn’t really forward the discussion.

    I’m just asking: what is the design take on the different genome sizes?

    How is that arguing against the design inference? Or delving into theocratic issues?

    Just looking over the other info . . . has anyone in baraminology created a kinds grouping list?

  70. BA77: I agree, the fossil record is far from complete. Which is why it’s considered only one thread in the rope supporting common descent with modification. Several biologists have even said that descent could be established without any fossils whatsoever.

    And, who knows, new fossils are being found every day.

    But you know all the arguments. So I’ll stop now.

  71. I was trying to find stuff about design and genome length and found a review of Dr Dembski’s Intelligent Design by Gert Korthof wherein he states:

    “Dembski defines Complex Specified Information, CSI, as “any specified information whose complexity exceeds 500 bits of information” (p166). Chance cannot generate CSI. However he didn’t translate that into a concrete DNA sequence length. I did not find it in his book. If he consulted Yockey he would have noticed that the cytochrome-c family of genes (113 amino acids, 339 bases long) has an information content of 233 – 373 bits. This is clearly lower than 500 bits. So although cytochrome-c undoubtedly contains information, it does not classify as CSI. So cytochrome-c is not an example of design and could be generated by chance according to Dembski’s criterion. This is a rather unexpected result. I don’t doubt Yockey’s calculation. Yockey made the most detailed calculation that can be found in the literature. Dembski knows Yockey’s book. It has far reaching consequences for Dembski’s design concept that cytochrome-c is not CSI. Because many genes have the same information content as cytochrome-c and many genes are below the 500 bits boundary. Thus many genes would not classify as CSI and would not be designed. Histone-H3 is just above the boundary (505 bits). The largest known mammalian gene, the dystrophin gene, contains 79 pieces (exons), is 2.4 Mb (Million bases) long, encodes a protein of 3685 amino acids and if the sequence is specified, it certainly must be designed. However Dembski did not mention any gene by name. The only concrete claim Dembski has made is: “the CSI of a flagellum far exceeds 500 bits” (p178), but there are about 50 genes involved in a flagellum. Why not claim that the human genome (estimated size: 3,2 billion base pairs; estimated number of genes: 30,000 – 40,000 25) far exceeds 500 bits? Why stop there? If there are now a standing diversity of 100 million biological species and each had a hundred thousand genes and genes in each species were at least slightly different from genes in all other species, then, not counting molecular diversity within species, the number of genes on planet Earth is 10 trillion. Dembski’s problem is: what units do we use? a piece of DNA? an exon? a gene? a gene family? a functional group of genes? a whole genome? all genomes on Earth?”

  72. And later in the same review:

    “Even if we assume that DNA contains Complex Specified Information (CSI), this does not answer the question: what real-life mechanism could produce CSI? Dembski concludes that natural law plus chance cannot explain information content in DNA. Is that true? To find out we must distinguish between two questions:

    1. is there a natural mechanism that creates the very first information (= origin of life)?
    2. can natural selection and mutation increase information content of DNA?

    Biologists don’t know all the details of the solution of the first question: the origin of life. The simplest free-living organism, Mycoplasma genitalium, has 468 genes. This would exceed Dembski’s boundary of 500 bits, I guess. Could this evolve gradually? We need data and experiments.

    Now the second question. Although Dembski tries to escape a positive answer to the second question, he finds himself saying: “selection introduces new information” (p177). Dembski also seems to accept that information can flow from the environment to an organism, thereby increasing the organism’s information content. Both statements contradict his main thesis that natural processes cannot generate CSI. On other pages he is so attached to the Law of Conservation of Information (‘Only Information begets Information’, p183) and the belief that CSI cannot be generated by natural processes, that he is forced to believe that CSI existed before the origin of life: CSI could be ‘abundant in the universe’ and ‘CSI is inherent in a lifeless universe’. This amounts to free-floating ghostly information in space, which is too far removed from down-to-earth biological science. The whole idea that information in DNA has any meaning outside living organisms is caused by pushing the information metaphor too far. The information in DNA is meaningless outside the cell. Just like the instructions in software do not have any meaning outside the very specific hardware environment in which they are executed. Further Dembski believes in ‘discrete insertions of CSI over time in organisms’ (p171). In that case I prefer Fred Hoyle’s panspermia theory, which is as unearthly but closer to observational science.”

  73. HA HA HA;

    ‘I agree, the fossil record is far from complete. Which is why it’s considered only one thread in the rope supporting common descent with modification. Several biologists have even said that descent could be established without any fossils whatsoever.’

    HA HA HA

    Thanks for the laugh :)

    “Now, after over 120 years of the most extensive and painstaking geological exploration of every continent and ocean bottom, the picture is infinitely more vivid and complete than it was in 1859. Formations have been discovered containing hundreds of billions of fossils and our museums now are filled with over 100 million fossils of 250,000 different species. The availability of this profusion of hard scientific data should permit objective investigators to determine if Darwin was on the right track. What is the picture which the fossils have given us? … The gaps between major groups of organisms have been growing even wider and more undeniable. They can no longer be ignored or rationalized away with appeals to imperfection of the fossil record.” Luther D. Sunderland, Darwin’s Enigma 1988, Fossils and Other Problems, 4th edition, Master Books, p. 9

    ellazimm,,,Man evolutionary science is easy, when any evidence is contrary to your hypothesis, just chuck the evidence, and rearrange all the remaining pieces to confirm your preferred presupposition.

    Is evolution pseudoscience?
    Excerpt:,,, Thus, of the ten characteristics of pseudoscience listed in the Skeptic’s Dictionary, evolution meets nine. Few other?pseudosciences — astrology, astral projection, alien abduction, crystal power, or whatever — would meet so many.
    http://creation.com/is-evolution-pseudoscience

    evanescence – lies – music video
    http://www.youtube.com/watch?v=XxHP9-fEuRk

  74. Joseph #61

    Has anyone ever done a complete side by side comparison of a human and chimp genome? And if not does anyone know what they are waiting for? Or do they not care what the real % difference is?

    If you with “side by side comparison” mean a pair-wise comparison of the chromosomes that would have no functional meaning because, for many reasons, the functional portions of a genome are never aligned with the similar functional portions of another genome.

    However just for curiosity I did such complete test between chimp and human and obtained an overall percentage of matching of 25.9%, which is almost exactly what the theory states. See my previous post, where I try to explain why genomic similarity is a very tricky and debatable issue.

  75. BA77: You’re very welcome. You should here my material on conservative politics! :-)

  76. niwrad could you help me understand this;

    However just for curiosity I did such complete test between chimp and human and obtained an overall percentage of matching of 25.9%, which is almost exactly what the theory states.

  77. niwrad, does the 25.9% matching have something to do with this fact?

    Jonathan Marks, (department of anthropology, University of California, Berkeley) has pointed out the often-overlooked problem with this “similarity” line of thinking.

    Because DNA is a linear array of those four bases—A,G,C, and T—only four possibilities exist at any specific point in a DNA sequence. The laws of chance tell us that two random sequences from species that have no ancestry in common will match at about one in every four sites. Thus even two unrelated DNA sequences will be 25 percent identical, not 0 percent identical (2000, p. B-7).

    Therefore a human and any earthly DNA-based life form must be at least 25% identical. Would it be correct, then, to state that daffodils are “one-quarter human”? The idea that a flower is one-quarter human is neither profound nor enlightening; it is outlandishly ridiculous! There is hardly any biological comparison that could be conducted that would make daffodils human—except perhaps DNA. Marks went on to concede:
    http://www.apologeticspress.or.....ticle=1038

  78. bornagain77 #77 … [!]

    Yes. It depends on the fact that the probability is 1/4 = 25%. To be precise it would be 25% only if the four signs A, T, G, C were identically probable and they are not. The theoretical value is 26%.

    By the way thank you for your massive engagement and contribution to my posts in particular and to the UD posts in general.

  79. BA77: I just want to note that I did try and honestly address your points as much as I’ve had time for but I’ve still got no response from you regarding the ID perspective on the wildly varied genome sizes found in nature. I admitted that I’ve got nothing new to add to the debate in support of my point and that you’ve heard it all before. And I’ve said many times that I really want to understand the stand that ID takes on certain issues. Which is why I’m here asking questions and NOT just making up responses based on my perceptions and bias.

    You frequently parade the fact that Darwinists can’t and won’t answer certain questions. Please be honest and acknowledge that there are some questions you can’t or choose not to answer.

    I haven’t got an agenda. I’m not a troll. I think we’d all benefit from understanding each other better.

  80. EZ:

    remember it is not just one protein in isolation that renders the verdict but he set of proteins involved in life. Yes, a 113 AA protein is within the search resources of the undirected cosmos, but when you look at the hundreds of co-ordinated proteins for life to work, the cumulative total is well beyond the threshold.

    GEM of TKI

  81. KF: Yes, that is clearly a major point, no question.

    I think the way the research has to go is first showing that small steps are achievable and then moving on to combinations. It will all take time.

    As I just mentioned in another thread, I’m kind of intrigued by the things that Lynn Margulis has attempted to establish. As a possible explanation for punctuated equilibrium, her hypotheses just might bridge some gaps. Thank goodness I should be around for a few more decades yet. I just might be lucky enough to see some of these deep questions answered!

    KF, you think about these things a lot . . . do you think Dr Dembski allowed for the flow of information from the environment to the organism? I can’t imagine that is the case myself.

  82. ellazimm, (said the spider to the fly)

    but anyways,,,

    I look at the varying genome sizes more generally, and perhaps someone with more expertise can give you a better more detailed answer,, but anyway for what its worth,,,

    ,,,As mentioned previously, the chimpanzee is found to have a 12% larger genome than humans. Thus, at first glance it would seem the chimpanzee is ‘more evolved’ than us humans, but this discrepancy is no anomaly of just chimps/humans. This disparity of genome sizes is found throughout life. There is no logical ‘evolutionary progression’ to be found for the amount of DNA in less complex animals to the size of genomes found in more complex animals. In fact the genome sizes are known to vary widely between Kinds/Species despite their differences in complexity and this mystery is known as the c-value enigma:

    C-value enigma
    Excerpt: it was soon found that C-values (genome sizes) vary enormously among species and that this bears no relationship to the presumed number of genes (as reflected by the complexity of the organism). For example, the cells of some salamanders may contain 40 times more DNA than those of humans. Given that C-values were assumed to be constant because DNA is the stuff of genes, and yet bore no relationship to presumed gene number, this was understandably considered paradoxical;
    http://en.wikipedia.org/wiki/C-value_enigma

    ,,, Thus contrary to Darwinian expectations of information being merely a ‘emergent’ property of various configurations of material particles there is no uniform progression to be seen from the sizes of genomes that would conform to this expectation of neo-Darwinism, whereas from an engineering perspective there are several reasons for why information may need to consolidated in one instance or to be more spread out in another instance. And depending on the level of ‘perfection’ to which the system is engineered, we should expect these considerations, which clearly we are not fully aware of yet, to be played out in excruciating detail!

  83. Upright: Genome size is a real puzzle. Thank you for responding. I think a design response has to be tentative at this point. Certainly the materialist view is provisional.

    Darwinian expectations would probably be: it happens, sometimes you gain lots of extra junk along the way, sometimes you don’t. But . . .

    Obviously a huge genome entails a certain amount of added resource spending, just to reproduce it for every cell. And if much of the genome is transcribed then . . . I’ve read some info about the energy expenditure involved but clearly more work needs to be done. Surely, at some point, the size of the genome alone would be selected against. Unless there’s some info therein which needs to be preserved.

    Have you ever thought how lucky we are to be around at a time when these questions are not only being examined but have a chance of being answered? Not only I am glad I was not born before tea but also that I am alive during a great explosion of knowledge. A Cambrian era of awareness?

    Thanks again for a stimulating day. I’ll be thinking about some of the things we discussed today for quite awhile and that is a very good thing. Especially some of Lynn Margulis’s points . . .

    Night all!

  84. Sorry, sorry, I was responding to BA77.

    DUH!!

    I really do apologise.

    I must be tired.

    Thank you for your time BA. If you ever come to visit York, England I’ll buy you a few pints of one of our finest ales. Promise.

    G’night!

  85. ellazimm, I’ve noticed that you seem to take comfort in Margulis’s points, which I believe are related to symbiosis, but the criticism I’ve seen leveled against here is that she is merely pushing the ‘information problem’ back a step by ‘shuffling around’ existing information, and she, like neo-Darwinists, never fully engages the question of ‘Where does the information come from in the first place?’

    As well, to your question on Dr. Dembski, though I’m surely out of my league here, from what I can tell Dr. Dembski and Dr. Marks have considered information coming from the ‘source of the environment’, as is reflected in this quote;

    “LIFE’S CONSERVATION LAW: Why Darwinian Evolution Cannot Create Biological Information”:
    Excerpt: Though not denying Darwinian evolution or even limiting its role in the history of life, the Law of Conservation of Information shows that Darwinian evolution is inherently teleological. Moreover, it shows that this teleology can be measured in precise information-theoretic terms.
    http://evoinfo.org/publication.....ation-law/

    ,,i.e. I believe Dr. Dembski is clearly stating that ‘IF’ Darwinian evolution occurred then the information needed to accomplish Darwinian evolution had to be built into the system.,,, Yet as far as observational science goes, the ‘environment’, has never been observed adding information over and above what was already present in a parent species, as is clearly illustrated by the fitness test which has never been passed by Darwinian processes, and as well as illustrated by Dr. Behe’s recent survey, and somewhat illustrated by Dr. Sanford’s work on Genetic Entropy:

    Is Antibiotic Resistance evidence for evolution? – ‘The Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net ‘fitness gain’ within a ‘stressed’ environment i.e. remove the stress from the environment and the parent strain is always more ‘fit’)
    http://behe.uncommondescent.co.....evolution/

    Michael Behe talks about the preceding paper on this podcast:

    Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time – December 2010
    http://intelligentdesign.podom.....3_46-08_00

    Evolution Vs Genetic Entropy – Andy McIntosh – video
    http://www.metacafe.com/watch/4028086

  86. BA77: Re: Lynn Margulis . . . I don’t know if solace is the right word . . . I find her ideas very interesting. I too suspect she is finding her ideas/cause in too many places. Not to say that what she’s proposing DOESN’T happen, probably not as much as she thinks it does. Worth following though. And, as you point out, she’s not answering some of your questions.

    I think I’m seeing the environment information issue more clearly now, thanks! I THOUGHT he was answering the question of where the information in the genome comes from in a different way.

    I know I’ve been frustrating to deal with but I really do have a better picture of what ID is really saying. Thanks again for taking the time.

  87. ellazimm you may find this recent post from Dr. Hunter interesting:

    From Philosopher to Science Writer: The Dissemination of Evolutionary Thought – May 2011
    Excerpt: The powerful theory of evolution hangs on this framework of thought that mandates naturalism. The science is weak but the metaphysics are strong. This is the key to understanding evolutionary thought. The weak arguments are scientific and the strong arguments, though filled with empirical observation and scientific jargon, are metaphysical. The stronger the argument, the more theological or philosophical.
    http://darwins-god.blogspot.co.....riter.html

    Dr. Hunter then goes on to cite an exact example of this ‘theology of Darwinism’,,, cited from a Darwinists writing on human genome, no less, which ties in very nicely with niwrad’s overarching subject for this thread.

    Oblivious to this context Farrell continues:

    But it’s even more problematic, Rice argues: the very structure of the genome itself—not just the mutations—is inconsistent with the idea that the genome, or the human body, or the world was directly designed by an external agent.

    The human genome is full of stuff that interferes with the use of genetic information to produce healthy and functional enzymes and bodies. First, consider the fact that only about 1 percent of human DNA codes for those enzymes. About 68 percent of the DNA consists of non-coding DNA that is between the genes, and about 31 percent of the DNA consists of non-coding DNA that is inside of the genes. This is, at best, a clumsy system, because whenever a cell divides, all of this DNA is copied, not just the DNA that the cell will use. In addition, since each gene is broken into little “exon” fragments by a large amount of internal “intron” DNA, the genetic information must be spliced together in order to be put to use. That is, to get a functional enzyme, the genetic information from lots of exon fragments has to be cobbled together. If it works, there is no problem, but the whole system is so cumbersomely complex that it often fails. Not only are many genetic diseases caused by mutations in the genes themselves, but many genetic diseases are caused by (or also caused by) failures of the cell to deal properly with the non-coding DNA and the splicing.

  88. niwrad, suppose chimp DNA was 99% identical to human DNA. That would mean that on the average, one in every 100 base pairs wouldn’t match up. Further, assume that the mismatched base pairs are randomly spread throughout the DNA.

    If you were comparing 100 base pair sections of DNA, almost every section would have a mismatch and your test would say that there was almost no simiilarity between chimp and human DNA.

    If you were comparing 50 base pair sections of DNA, then on average, every other section would have a mismatch and your test would report that chimp and human DNA varied by 50 percent.

    If you were comparing 25 base pair sections of DNA, on average every fourth section would have a mismatch and your test would report that chimp and human DNA was 25% different.

    And if you compared sections that were one base pair long, your test would report that on the average, every 100th section had a mismatch and human and chimp DNA were thus 99% identical.

    The problem is with your test. The bigger the sections of DNA that your compare, the more likely the sections are to contain a mismatch and the lower the similarity between chimp and human DNA it will report.

  89. Thank you bornagain77 and niwrad-

    Interesting.

  90. dmullenix you state;

    ‘And if you compared sections that were one base pair long, your test would report that on the average, every 100th section had a mismatch and human and chimp DNA were thus 99% identical.’

    This simply is not true, in fact as has been pointed out several times on this very thread. the only way that neo-Darwinists have been able to hood-wink the general public that we were 98.8% genetically similar is by ignoring vast swaths of DNA that did not match similarity.

    notes:

    The Unbearable Lightness of Chimp-Human Genome Similarity
    Excerpt: One can seriously call into question the statement that human and chimp genomes are 99% identical. For one thing, it has been noted in the literature that the exact degree of identity between the two genomes is as yet unknown (Cohen, J., 2007. Relative differences: The myth of 1% Science 316: 1836.). ,,, In short, the figure of identity that one wants to use is dependent on various methodological factors.
    http://www.evolutionnews.org/2......html#more

    Chimpanzee?
    10-10-2008 – Dr Richard Buggs – research geneticist at the University of Florida
    …Therefore the total similarity of the genomes could be below 70%.
    http://www.idnet.com.au/files/pdf/Chimpanzee.pdf

    A False Trichotomy
    Excerpt: The common chimp (Pan troglodytes) and human Y chromosomes are “horrendously different from each other”, says David Page,,, “It looks like there’s been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages.”
    http://www.uncommondescent.com.....richotomy/

    Do Human and Chimpanzee DNA Indicate an Evolutionary Relationship?
    Excerpt: the authors found that only 48.6% of the whole human genome matched chimpanzee nucleotide sequences. [Only 4.8% of the human Y chromosome could be matched to chimpanzee sequences.]
    http://www.apologeticspress.org/articles/2070

    etc.. etc…

  91. “The problem is with your test. The bigger the sections of DNA that your compare, the more likely the sections are to contain a mismatch and the lower the similarity between chimp and human DNA it will report.”

    Which isn’t to say it doesn’t work. It seems efficient and consistant. It is just necessary have to have a correction factor-dividing the 30bp metric by 24 gives the real percent mismatch. I mention this in post 2 in this thread.

    It is pretty easy to derive why you’d divide by 24-but the most straightforward demonstration might be to generate test genomes with 0.1, 1, 2, and 3 percent difference. The results will be about 2.4, 24, 48 and 72% difference on the 30 bp metric. I think a 4% mismatch will give nearly 0% similarity.

    Without the correction, the 30bp metric amplifies dissimilarity compared to regular matching,

  92. BA:
    Whatever you link here in your usual fashion, it has no bearing on the argument of dmullenix. It´s a fact that the procedure devised by niwrad is rather pointless if you don´t correct your output values with respect to the length of the strings you compare.
    So you completely miss the point. Whatever the real difference is, niwrads method can only be used to determine it if the effect of the length of the strings is taken into account.

  93. Indium, but of coarse I have no bearing for you because it is not a answer you want to hear, but regardless of the answer you want, let’s take a closer look and see that it gets worse for you. If we use dmullenix example here,

    ‘‘And if you compared sections that were one base pair long, your test would report that on the average, every 100th section had a mismatch and human and chimp DNA were thus 99% identical.’

    We find dmullenix to completely miss the point for niwrad did exactly this test and found;

    ‘If you with “side by side comparison” mean a pair-wise comparison of the chromosomes that would have no functional meaning because, for many reasons, the functional portions of a genome are never aligned with the similar functional portions of another genome.

    However just for curiosity I did such complete test between chimp and human and obtained an overall percentage of matching of 25.9%, which is almost exactly what the theory states. See my previous post, where I try to explain why genomic similarity is a very tricky and debatable issue.’

    But of coarse you will cry foul, but the point is that the exact test dmullenix specified gives a 25.9% reading

  94. i.e. Just who gets to choose which parts of the genome to consider and why??? i.e. My exact point is that neo-Darwinists are EXTREMELY biased as to exactly which parts of the genome they will consider and which points they won’t.,,, Not an answer you want is it??? :) TOO BAD!!!

  95. “i.e. Just who gets to choose which parts of the genome to consider and why??? i.e. My exact point is that neo-Darwinists are EXTREMELY biased as to exactly which parts of the genome they will consider and which points they won’t.,,, Not an answer you want is it??? TOO BAD!!!”

    Umm…as Nirwad states:

    “The test is purely statistical, it doesn’t take into account moves, introns, orphans and any functional concept.”

    He didn’t game the data before his alignment, and the corrected 30bp metric gives 98.4% identity between chimps and humans. There are different values out there-very high if we align only ORFs (this is where a 99+% comes from-when that was the only data available-lower if you count different numbers of transposons and deletions and such as mismatches. I’ve seen values for a total nt to nt comparison that come up with something like 96%.

    I’ve explained twice now why the values that get to 70% or lower are just wrong. The chimpanzee genome draft was built using a human scaffold. Initially, a large percentage of sequences (at low coverage) could not unambiguously be assigned–usually because they were repeat sequences that could match multiple places. These unmatched bits have dropped with more sequence, and better placement. Any way you pick and choose, the similarities are very high.

    And if you use a consistant process (even the 30bp metric!), the difference will increase with phylogenetic distance. This is more significant than the absolute number!

  96. Sorry, I looked at the wrong number.

    If we take:

    “However just for curiosity I did such complete test between chimp and human and obtained an overall percentage of matching of 25.9%,”

    And correct it by dividing by 24, that is 1.079% different, or 98.9% identity.

  97. DrREC, (using the Fit DAMN YOU FIT!!! method of science),,, but of coarse, what else should I expect from a man who fully endorses this following study;

    This following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 ‘ORFan’ genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!

    Human Gene Count Tumbles Again – 2008
    Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes.
    http://www.sciencedaily.com/re.....161406.htm

    The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. But DrREC fully endorses the method in post number 20 calling it ‘reasonable’; Well regardless of how reasonable DThis following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 ‘ORFan’ genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!

    Human Gene Count Tumbles Again – 2008
    Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes.
    http://www.sciencedaily.com/re.....161406.htm

    The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. DrREC perceives himself to be the fact of the matter, If the authors of the preceding study were to have actually tried to see if the over 1000 unique ORFan genes of humans may actually encode for proteins, instead of just written them off because they were not found in other supposedly related species, they would have found that there is ample reason to believe that they may very well encode for biologically important proteins:

    A survey of orphan enzyme activities
    Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles.
    http://www.biomedcentral.com/1471-2105/8/244

    Dr. Howard Ochman – Dept. of Biochemistry at the University of Arizona
    Excerpt of Proposal: Although it has been hypothesized that ORFans might represent non-coding regions rather than actual genes, we have recently established that the vast majority that ORFans present in the E. coli genome are under selective constraints and encode functional proteins.
    http://www.uncommondescent.com.....ent-358868

    In fact it turns out that the authors of the ‘kick the ORFans out in the street’ paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias:
    http://www.uncommondescent.com.....ent-358547

    Moreover the ‘anomaly’ of unique ORFan genes is found in every new genome sequenced:

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    As well, completely contrary to evolutionary thought, these ‘new’ ORFan genes are found to be just as essential as ‘old’ genes for maintaining life:

    Age doesn’t matter: New genes are as essential as ancient ones – December 2010
    Excerpt: “A new gene is as essential as any other gene; the importance of a gene is independent of its age,” said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. “New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked.”
    http://www.sciencedaily.com/re.....142523.htm

    New genes in Drosophila quickly become essential. – December 2010
    Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages.
    http://www.sciencemag.org/cont.....2.abstract

    I would like to reiterate that evolutionists cannot account for the origination of even one unique gene or protein, much less the over one thousand completely unique ORFan genes found distinctly imbedded within the 20,000 genes of the human genome:

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

    “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: – Doug Axe ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences.”
    http://www.mendeley.com/resear.....yme-folds/

  98. DrREC, (with sledge hammer, using the Fit, DAMN YOU, FIT!!! method of science to arrive at his desired conclusion),,, but of coarse DrREC, what else should I expect from a man who fully endorses the extreme bias of this following study;

    This following article, which has a direct bearing on the 98.8% genetic similarity myth, shows that over 1000 ‘ORFan’ genes, that are completely unique to humans and not found in any other species, and that very well may directly code for proteins, were stripped from the 20,500 gene count of humans simply because the evolutionary scientists could not find corresponding genes in primates. In other words evolution, of humans from primates, was assumed to be true in the first place and then the genetic evidence was directly molded to fit in accord with their unproven assumption. It would be hard to find a more biased and unfair example of practicing science!

    Human Gene Count Tumbles Again – 2008
    Excerpt: Scientists on the hunt for typical genes — that is, the ones that encode proteins — have traditionally set their sights on so-called open reading frames, which are long stretches of 300 or more nucleotides, or “letters” of DNA, bookended by genetic start and stop signals.,,,, The researchers considered genes to be valid if and only if similar sequences could be found in other mammals – namely, mouse and dog. Applying this technique to nearly 22,000 genes in the Ensembl gene catalog, the analysis revealed 1,177 “orphan” DNA sequences. These orphans looked like proteins because of their open reading frames, but were not found in either the mouse or dog genomes. Although this was strong evidence that the sequences were not true protein-coding genes, it was not quite convincing enough to justify their removal from the human gene catalogs. Two other scenarios could, in fact, explain their absence from other mammalian genomes. For instance, the genes could be unique among primates, new inventions that appeared after the divergence of mouse and dog ancestors from primate ancestors. Alternatively, the genes could have been more ancient creations — present in a common mammalian ancestor — that were lost in mouse and dog lineages yet retained in humans. If either of these possibilities were true, then the orphan genes should appear in other primate genomes, in addition to our own. To explore this, the researchers compared the orphan sequences to the DNA of two primate cousins, chimpanzees and macaques. After careful genomic comparisons, the orphan genes were found to be true to their name — they were absent from both primate genomes.
    http://www.sciencedaily.com/re.....161406.htm

    The sheer, and blatant, shoddiness of the science of the preceding study should give everyone who reads it severe pause whenever, in the future, someone tells them that genetic studies have proven evolution to be true. DrREC perceives himself to be the fact of the matter, If the authors of the preceding study were to have actually tried to see if the over 1000 unique ORFan genes of humans may actually encode for proteins, instead of just written them off because they were not found in other supposedly related species, they would have found that there is ample reason to believe that they may very well encode for biologically important proteins:

    A survey of orphan enzyme activities
    Abstract: We demonstrate that for ~80% of sampled orphans, the absence of sequence data is bona fide. Our analyses further substantiate the notion that many of these (orfan) enzyme activities play biologically important roles.
    http://www.biomedcentral.com/1471-2105/8/244

    Dr. Howard Ochman – Dept. of Biochemistry at the University of Arizona
    Excerpt of Proposal: Although it has been hypothesized that ORFans might represent non-coding regions rather than actual genes, we have recently established that the vast majority that ORFans present in the E. coli genome are under selective constraints and encode functional proteins.
    http://www.uncommondescent.com.....ent-358868

    In fact it turns out that the authors of the ‘kick the ORFans out in the street’ paper actually did know that there was unbiased evidence strongly indicating the ORFan genes encoded proteins but chose to ignore it in favor of their preconceived evolutionary bias:
    http://www.uncommondescent.com.....ent-358547

    Moreover the ‘anomaly’ of unique ORFan genes is found in every new genome sequenced:

    Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
    http://www.vimeo.com/17135166

    As well, completely contrary to evolutionary thought, these ‘new’ ORFan genes are found to be just as essential as ‘old’ genes for maintaining life:

    Age doesn’t matter: New genes are as essential as ancient ones – December 2010
    Excerpt: “A new gene is as essential as any other gene; the importance of a gene is independent of its age,” said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. “New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked.”
    http://www.sciencedaily.com/re.....142523.htm

    New genes in Drosophila quickly become essential. – December 2010
    Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages.
    http://www.sciencemag.org/cont.....2.abstract

    I would like to reiterate that evolutionists cannot account for the origination of even one unique gene or protein, much less the over one thousand completely unique ORFan genes found distinctly imbedded within the 20,000 genes of the human genome:

    Could Chance Arrange the Code for (Just) One Gene?
    “our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236).”
    http://www.creationsafaris.com/epoi_c10.htm

    ,,, So DrREC, since similarity evidence is taken away from you, do you now want to go back over the fact that you have no foundation in science to begin with for your neo-Darwinian conjectures???

  99. DrREC, this has me scratching my head at the sheer absurdity of it all. You actually stated this:

    ”“However just for curiosity I did such complete test between chimp and human and obtained an overall percentage of matching of 25.9%,”

    And correct it by dividing by 24, that is 1.079% different, or 98.9% identity.”

    But DrREC 25.9% is the number you should get when you compare ANY two random genomes together. So does that mean if I were to use your ’24′ correction factor’ on a daffodil genome, that matches human genomes to 25.9%, then it would then give the ‘Correct’ reading of 98.9% identity. Why DrREC, that’s just so special. Not that I don’t appreciate your ‘creative accounting/math skills’, but How about we look at a little more rigorous math to see what neo-Darwinism is up against to ‘fix’ JUST a single beneficial mutation within the hypothesized human lineage???

    Waiting Longer for Two Mutations – Michael J. Behe
    Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.
    http://www.discovery.org/a/9461

    Dr. Sanford calculates it would take 12 million years to “fix” a single base pair mutation into a population. He further calculates that to create a gene with 1000 base pairs, it would take 12 million x 1000 or 12 billion years. This is obviously too slow to support the creation of the human genome containing 3 billion base pairs.
    http://www.detectingtruth.com/?p=66

    Whale Evolution Vs. Population Genetics – Richard Sternberg PhD. in Evolutionary Biology – video
    http://www.metacafe.com/watch/4165203

    further notes:

    “No human investigation can be called true science without passing through mathematical tests.”
    Leonardo Da Vinci

    God by the Numbers – Charles Edward White
    Excerpt: “Even if we limit the number of necessary mutations to 1,000 and argue that half of these mutations are beneficial, the odds against getting 1,000 beneficial mutations in the proper order is 2^1000. Expressed in decimal form, this number is about 10^301. 10^301 mutations is a number far beyond the capacity of the universe to generate. Even if every particle in the universe mutated at the fastest possible rate and had done so since the Big Bang, there still would not be enough mutations.”
    http://www.christianitytoday.c.....ml?start=2

    Indeed, math is not kind to Darwinism in the least when considering the probability of humans ‘randomly’ evolving:

    In Barrow and Tippler’s book The Anthropic Cosmological Principle, they list ten steps necessary in the course of human evolution, each of which, is so improbable that if left to happen by chance alone, the sun would have ceased to be a main sequence star and would have incinerated the earth. They estimate that the odds of the evolution (by chance) of the human genome is somewhere between 4 to the negative 180th power, to the 110,000th power, and 4 to the negative 360th power, to the 110,000th power. Therefore, if evolution did occur, it literally would have been a miracle and evidence for the existence of God. William Lane Craig

    William Lane Craig – If Human Evolution Did Occur It Was A Miracle – video
    http://www.youtube.com/watch?v=GUxm8dXLRpA

    Along that same line:

    Darwin and the Mathematicians – David Berlinski
    “The formation within geological time of a human body by the laws of physics (or any other laws of similar nature), starting from a random distribution of elementary particles and the field, is as unlikely as the separation by chance of the atmosphere into its components.”
    Kurt Gödel, was a preeminent mathematician who is considered one of the greatest to have ever lived. Of Note: Godel was a Theist!
    http://www.evolutionnews.org/2.....cians.html

    “Darwin’s theory is easily the dumbest idea ever taken seriously by science.”
    Granville Sewell – Professor Of Mathematics – University Of Texas – El Paso

  100. “But DrREC 25.9% is the number you should get when you compare ANY two random genomes together.”

    NOT for the 30-bp metric. Anything more than ~4% difference will yield a score of 0.

    By the way, this 25.9% is a nt to nt metric that assumes a 1 out of 4 chance of matching, adjusted for composition bias. In reality, longer alignments are required for the ‘matches’ we’re talking about, so scores will go to 0-or no alignment.

    Again, the sequences are public-please do try it yourself!

    “So does that mean if I were to use your ’24? correction factor’ on a daffodil genome, that matches human genomes to 25.9% then it would then give the ‘Correct’ reading of 98.9% identity.”

    Human-daffodil homology is probably significantly higher than that-but NOT for the 30bp metric, which will give almost no matches. You’re applying the correction for the 30bp metric to a non-30 bp metric, which yeah, gives silly results.

    “Why DrREC, that’s just so special. Not that I don’t appreciate your ‘creative accounting/math skills’”

    I’m just providing the correction factor for niwrad’s metric. It is really clear that increasing string length will increase mismatch. For example, if we used a search of over 1000 bases, and demanded 100% identity for a match, than most humans would have 0% homology to any other human, given our 0.1% differences! I’m not the one being ‘creative’ here, just providing the correction factor to mathematics that could otherwise be creatively, ahem, interpreted.

  101. Why DrREC, I am very certain the only one being very creative with there interpretation is YOU!!! No matter what the evidence says you will disregard anything that falsifies neo-Darwinism and exagerate anything that can be twisted to your neo-Darwinian bias. You could care less to establish a rigorous foundation to see what is actually true, for the conclusion is far to important to you to be left to the evidence to decide!!,,,

    you presuppose the human genome is just a cobbled together piece of junk don’t you??? put together by a trial a error process don’t you? Whereas I think God originally created the Human genome! Let’s look at a few points of trivia, and see whose view more accurately reflects reality?!?

    Man has over 3 billion base pairs of DNA code. The average number of cells in the human body is between 75 and 100 trillion cells. 300 million cells in the human body die and are replaced (most of them) every minute. If all the DNA was removed from a single cell in a person’s body and laid end to end, it would be six feet long. If the DNA was removed from all of the cells in a person’s body and laid end to end, it would stretch from Earth to the sun and back 450 times, or about 135 billion kilometers. The human genome, according to Bill Gates the founder of Microsoft, far, far surpasses, in complexity, any computer program ever written by man. The data compression (multiple meanings) of some stretches of human DNA is estimated to be up to 12 codes thick! (Trifonov, 1989) No line of computer code ever written by man approaches that level of data compression (poly-functional complexity). There are about three-billion letters of code on the six feet of DNA curled up in each human cell. The amount of information in human DNA is roughly equivalent to 12 sets of The Encyclopaedia Britannica—an incredible 384 volumes worth of detailed information that would fill 48 feet of library shelves! If you were to read the code aloud, at a rate of three letters per second for twenty-four hours per day (about one-hundred-million letters a year), it would take you over thirty years to read it. Looking at all the digital and analog memory devices in the world, researchers calculated in 2011 that humankind is able to store at least 295 exabytes of information (that’s a number with 20 zeroes in it), but that is still less than one percent of the information that is stored in all the DNA molecules of a single human being. The capacity of a DNA molecule to store information is so efficient that all the information needed to specify an organism as complex as man weighs less than a few thousand-millionths of a gram. The information in the DNA of all the different species of organisms which have ever existed on earth (a number estimated to be one billion) could easily fit into a teaspoon with plenty of room left over for every book ever written on the face of the earth. For comparison sake, if mere man were to try to ‘quantum teleport’ just one human body (change a physical human body into “pure information” and then ‘teleport’ it to another physical location) it would take at least 10^32 bits just to decode the teleportation event, or a cube of CD-ROM disks 1000 kilometers on 1 side, and would take over one hundred million centuries to transmit all that information for just one human body even with the best optical fibers conceivable!
    (A fun talk on teleportation – Professor Samuel Braunstein -
    http://www.research.ibm.com/qu.....stein.html)

    “To the skeptic, the proposition that the genetic programmes of higher organisms, consisting of something close to a thousand million bits of information, equivalent to the sequence of letters in a small library of 1,000 volumes, containing in encoded form countless thousands of intricate algorithms controlling, specifying, and ordering the growth and development of billions and billions of cells into the form of a complex organism, were composed by a purely random process is simply an affront to reason. But to the Darwinist, the idea is accepted without a ripple of doubt – the paradigm takes precedence!”
    Michael Denton

    Psalm 139: 14-15
    “I praise you because I am fearfully and wonderfully made;,,, When I was woven together in the depths of the earth, your eyes saw my unformed body.”

    ============

    Human Genome “Infinitely More Complex” Than Expected – April 2010
    Excerpt: Hayden acknowledged that the “junk DNA” paradigm has been blown to smithereens. “Just one decade of post-genome biology has exploded that view,” she said,,,, Network theory is now a new paradigm that has replaced the one-way linear diagram of gene to RNA to protein. That used to be called the “Central Dogma” of genetics. Now, everything is seen to be dynamic, with promoters and blockers and interactomes, feedback loops, feed-forward processes, and “bafflingly complex signal-transduction pathways.”
    http://www.creationsafaris.com.....#20100405a

    Scientists Map All Mammalian Gene Interactions – August 2010
    Excerpt: Mammals, including humans, have roughly 20,000 different genes.,,, They found a network of more than 7 million interactions encompassing essentially every one of the genes in the mammalian genome.
    http://www.sciencedaily.com/re.....142044.htm

    etc..etc..

    DrREC, whose presupposition is supported by the evidence and whose is not?

  102. “2011 that humankind is able to store at least 295 exabytes of information (that’s a number with 20 zeroes in it), but that is still less than one percent of the information that is stored in all the DNA molecules of a single human being.”

    Hah-more fun with math.

    You only get there if you multiple the human genome by the 50 trillion cells in the human body. Of course, these are absolutely duplicate copies!

    So scratch that, and you’re down to quite a few less zeros. Human chromosome 1, with all annotations, is about 295 Mb unzipped.

    You can download it here:

    ftp://ftp.ncbi.nlm.nih.gov/gen.....hr1.gbk.gz

    The whole genome fits comfortably on a DVD.

  103. DrREC,,, grits teeth, ignores all evidence of stunning craftsmanship, and with pure atheistic indignation says with scoffing defiant tone,,, TIS JUNK I TELL YA, JUNK, JUNK, JUNK!!! :)

    Romans 1:20-23
    For since the creation of the world God’s invisible qualities—his eternal power and divine nature—have been clearly seen, being understood from what has been made, so that people are without excuse. For although they knew God, they neither glorified him as God nor gave thanks to him, but their thinking became futile and their foolish hearts were darkened. Although they claimed to be wise, they became fools and exchanged the glory of the immortal God for images made to look like a mortal human being and birds and animals and reptiles.

  104. 104

    “The whole genome fits comfortably on a DVD … all encoded in an inert system of symbols whose physical bonds do not determine the sequence in which they exist, nor the method in which they are to be decoded.”

    There Doc, I fixed that for ya!

    Now if we can just get a DVD to fit inside the nucleus of a cell.

  105. bornagain77 and Upright-

    Funny responses! Particularly for BA77-when the science becomes frustrating, throw bible quotes at me?

    Did I say anything about design, junk, or God? Just getting the math straight. Not making analogies about how the information is stored or comes from.

    And again, if anyone wants to prove me wrong, what are the 30bp metrics for a test set designed with 0.1%, 1%, 2%, and 4% differences?

    What are the 30bp metrics for humans, chimps, gorillas and orangutans? The gorilla is fairly draft-but should suffice for this purpose.

    My predictions are:

    1) You’ll derive a easy factor to convert 30bp metric to a real percent difference.

    3) 30bp metric differences (despite being amplified) will be phylogenetically consistant.

  106. DrREC, what a laugh, you don’t even have a foundation in science to begin to make your neo-Darwinian conjectures with, and completely ignore that SCIENTIFIC fact, and then pretend as if you are being reasonable when you make completely unfounded conjectures as to what you want the percentage to be. And then you, having failed to have me fall for your ruse of creative accounting, have the audacity to label me as being unscientific for not accepting your atheistic games???

  107. 107

    Doc, I just thought your throwaway line needed a bit more substance.

    And I have a prediction of my own. I predict that man will create artificial life from living precusors before we’ll stumble upon a way where inanimate matter can instantiate an abstraction of a discrete state into an information medium by the use of inert digital symbols – and – create rules by which it can be decoded … but, of course, thats just me.

    -cheers

  108. DrREC, in case you sneeze, God Bless you!

    Dane Cook – Sneezing Atheist – video
    http://www.youtube.com/watch?v=TXtVzj9y-bo

  109. ” when you make completely unfounded conjectures as to what you want the percentage to be. And then you, having failed to have me fall for your ruse of creative accounting, have the audacity to label me as being unscientific for not accepting your atheistic games???”

    Ok-lets start simple. 10 differences in a linear string of 1000. If we use a 1 nt metric this is 99% identical. If we use 1000 it will ~zero. A 10 nt metric will give about 90%, if I’m doing the math right.

    Are we agreed that the size of the search string skews the percent similarity?

    And BA77-can we dispense with the atheism remarks. I don’t know why my attempts to get facts straight with my faith.

  110. “And I have a prediction of my own. I predict that man will create artificial life from living precusors before we’ll stumble upon a way where inanimate matter can instantiate an abstraction of a discrete state into an information medium by the use of inert digital symbols – and – create rules by which it can be decoded … but, of course, thats just me.”

    Another ID postdiction!
    http://www.guardian.co.uk/scie.....-life-form

  111. 111

    Ahh…an rhetorical opportunist!

    I applaud.

    Actually I was thinking a bit deeper than what Venter has marvelously accomplished thusfar, but the point is the same.

    We will not get a symbolicly encoded abstraction of a discrete state instantiated into a material medium (along with the rules for decoding it) until we do it ourselves. Why? Because an act of agency is the mechanism by which such things come about.

    In the vacuum of demonstrable evidence otherwise, I like my chances.

  112. DrREC, ,,, What preferred string are you counting from and why???. Are you counting the over 1000 completely unique human genes??? Or is that just so much to be hid under the rug??? My whole point DrREC, is that you cannot just pick and choose which strings are to be included in your count! It is completely biased for neo-Darwinists to be allowed to only keep that which matches their preconceived bias!!! For a man who has such a high opinion of his own intelligence, you sure seem to have a hard time with such a simple point!!! All unbiased counts are significantly lower that your ‘preferred’ count, but you insist they are not counting correctly but you are. WHY??? Because it does not match your preconceived conclusion is why you insist this is so. Tell you what DrREC, to be fair with your line of reasoning, let us throw out everything that doesn’t match from the kangaroo genome and see how close to 99% we can get. Deal??

    Kangaroo genes close to humans
    Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
    http://www.reuters.com/article.....P020081118

    -

    DNA Comparisons between Humans and Chimps – Fazale Rana
    Excerpt: It is interesting that when evolutionary biologists discuss genetic comparisons between human and chimpanzee genomes, the fact that, again, as much as 25 percent of the two genomes won’t align receives no mention. Instead, the focus is only on the portions of the genome that display a high-degree of similarity. This distorted emphasis makes the case for the evolutionary connection between humans and chimps seem more compelling than it may actually be.
    http://www.reasons.org/dna-com.....del-part-2

    Moreover DrREC, why don’t you face the following crushing evidence straight on instead of just ignoring it because it does not fit your neo-Darwinian worldview???

    The mouse is not enough – February 2011
    Excerpt: Richard Behringer, who studies mammalian embryogenesis at the MD Anderson Cancer Center in Texas said, “There is no ‘correct’ system. Each species is unique and uses its own tailored mechanisms to achieve development. By only studying one species (eg, the mouse), naive scientists believe that it represents all mammals.”
    http://www.the-scientist.com/news/display/57986/

    The Origin at 150: is a new evolutionary synthesis in sight? – Koonin – Nov. 2009
    Excerpt: The edifice of the modern synthesis has crumbled, apparently, beyond repair.
    http://www.arn.org/blogs/index....._synthesis

    Modern Synthesis of Neo-Darwinism Is Dead – Paul Nelson – video
    http://www.metacafe.com/watch/5548184/

    further note:

    Why The Chromosomal Fusion Argument Doesn’t Wash – Jonathan M – February 2011
    http://www.uncommondescent.com.....esnt-wash/

    Recent Genetic Research Shows Chimps More Distant From Humans,,, – Jan. 2010
    Excerpt: A Nature paper from January, 2010 titled, “Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content,” found that Y chromosomes in humans and chimps “differ radically in sequence structure and gene content,” showing “extraordinary divergence” where “wholesale renovation is the paramount theme.”,,, “Even more striking than the gene loss is the rearrangement of large portions of the chromosome. More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa,,,”
    http://www.evolutionnews.org/2.....shows.html

    etc.. etc..

    So DrREC to make it real clear how pointless your argument is,,, let’s rephrase it a bit to reflect where you are actually at as far as a solid foundation in science is concerned,,,, let’s make it real simple! :) ,,, we got a string of 1000, only 20 match, ,,, what does that make the price of tea in China???

  113. DrREC, please tell me exactly how many unique proteins and/or genes Venter created from scratch when he synthesized (copied) a genome and inserted it into a bacterium???

    Jeopardy Theme
    http://www.youtube.com/watch?v=0Wi8Fv0AJA4

  114. Of related interest:

    Skittle: A 2-Dimensional Genome Visualization Tool – Josiah D Seaman and John C Sanford

    Excerpt: Background

    It is increasingly evident that there are multiple and overlapping patterns within the genome, and that these patterns contain different types of information – regarding both genome function and genome history. In order to discover additional genomic patterns which may have biological significance, novel strategies are required. To partially address this need, we introduce a new data visualization tool entitled Skittle.
    Results

    This program first creates a 2-dimensional nucleotide display by assigning four colors to the four nucleotides, and then text-wraps to a user adjustable width. This nucleotide display is accompanied by a “repeat map” which comprehensively displays all local repeating units, based upon analysis of all possible local alignments. Skittle includes a smooth-zooming interface which allows the user to analyze genomic patterns at any scale.

    Skittle is especially useful in identifying and analyzing tandem repeats, including repeats not normally detectable by other methods. However, Skittle is also more generally useful for analysis of any genomic data, allowing users to correlate published annotations and observable visual patterns, and allowing for sequence and construct quality control.
    Conclusions

    Preliminary observations using Skittle reveal intriguing genomic patterns not otherwise obvious, including structured variations inside tandem repeats. The striking visual patterns revealed by Skittle appear to be useful for hypothesis development, and have already led the authors to theorize that imperfect tandem repeats could act as information carriers, and may form tertiary structures within the interphase nucleus.
    http://www.biomedcentral.com/1471-2105/10/452

    Perhaps if some neo-Darwinists were not so busy trying to cram the ‘junky’ genome into their preconceived conclusions, they would have thought of such a elegant way to analyze the genome???

    Just a thought DrREC!

  115. All,

    DrREC is correct that the value you use for number of bases compared will affect the similarity results, not giving true similarity.

    For example, the following (ugly) python code shows this:

    #=================
    from __future__ import division
    import numpy as np
    import random

    m = 30
    x = list(np.random.randint(0, 4, 1000))
    y = [i if np.random.binomial(1, 0.99) else \
    random.sample(set(range(0,4)).symmetric_difference([i]), 1)[0] \
    for i in x]
    samples = 10000
    offsets = [np.random.randint(0, len(x)-m) for j in range(0, samples)]
    print sum([x[i:i+m] == y[i:i+m] for i in offsets]) / samples
    #=================

    If you set m = 1, you get roughly the correct 0.99 similarity. (Notice the 0.99 binomial threshold, which should make y a close to 99% identical copy of x). Now let m = 30. The similarity drops to about 70%.

    My method is slightly different, in that I know exactly where the 30bp section should begin in the second genome, so I don’t perform a search to find it. (If the m window is small enough, you may find spurious matches due to random chance.)

    Anyway, DrREC, how did you derive your correction factor? You’re right that the windowed-probabilistic matching does give incorrect similarity results, but I don’t see how your correction factor is the fix.

    Atom

    Sorry ‘niwrad’[::-1], I enjoy your posts. DrREC just has made a valid point.

  116. PS the code assumes a version of python < 3.0, with the numpy package installed. This shouldn't be too difficult to code in matlab, if you don't have python installed.

  117. Well DrREC, though I surely don’t buy how you have tried to nudge things to reflect your desired percentages in the end results, nor the way you have handled related evidence presented to you, I do have to apologize to you if Atom thinks you may have a valid point as to the methodology.,,, And for that I am sorry.

  118. A note on the dividing by 24 ‘correction factor.’

    CharlesJ, the last time this was brought up, introduced the use of the a probability calculator to convert from 30bp metric to real percent mismatch.

    The calculator approach works really really well-if you take this for example: http://stattrek.com/Tables/Binomial.aspx
    and plug in, .01 (for 99% similarity), 30 trials, and 1 success, the Cumulative Probability: P(X < 1) will give the 30bp metric for any value. So 99% similar becomes 74%, 98% becomes 54% and so on. Atom's empirical trial is consistant with this result.

    Taking these values, CharlesJ adopted a conversion-dividing the percent mismatch by 24 to 'fix' the 30bp metric, which I mis-remembered as being a far more accurate a conversion than it is-it is actually only accurate only for a small range of values, as far as I can tell.

    So bit of a mis-remember there on what actually worked.

    As the last thread closed, I think even niwrad was in agreement a conversion was necessary.

    The correct conversion, as Joe Felsenstein has now pointed out, is to take the actual percent match and raise it to the 30th power. The values that result are exactly that given the use of the calculator by CharlesJ's (as they should be!).

    So for 99% matching, .99^30 gives 0.739.

    The dirty back-conversion would be 1-.739=.261 .261/24=.0011 difference ~99% identical

    The accurate conversion is taking the 30th root of the 30bp metric.

  119. Everybody spot the extra zero? That’s a typo, not the math!

  120. DrREC, excuse me but that’s all french to me, so using this method, what is the bottom line for you?? What is the actual percentage difference you are trying to claim? ,,, And a question more to my ballpark, what is your empirical evidence that the changes you require can be accomplished if genetic reductionism were true??

    ==============

  121. OK DrRec, that makes more sense. Since the error didn’t appear to be a constant multiple I was confused at how linear scaling could fix it. Running at a few different values, I was getting increasing differences between actual difference and estimated difference (using niwrad’s method). When I thought through what niwrad was actually doing (taking binomial trials and looking for a large number of consecutive non-mutations) the constant correction factor of 24 proposed made even less sense.

    Thanks for explaining the correction factor. In the end, a few mistakes have been made in this little research experiment, by more than just niwrad. Hopefully we can all show some humility and just enjoy the fact that there are other nerds on the internet interested in applying math to biological problems. : ) Normal people don’t really care about these things, so it’s good to have other Darwinist and ID geeks to hash them out with.

    We all make math mistakes from time to time, no shame in that.

    Atom

  122. Another use of niwrad’s 30-base comparison could be to sniff out which chromosomes are the best match, if that was unknown or (in the case of kangaroos) the numbers were uneven.

    First we can see that the chance of matching a given sequence to a particular location in a random chromosome is tiny. It’s 1/(4^30), or roughly one chance in a million million million. So if we have a random chromosome that’s 100 million bases long, the chance of a match anywhere on that to our test sequence is one in ten billion. Effectively zero. So that makes the test that niwrad is undertaking strong evidence of matching.

    Looking at the chimpanzee example, we should easily be able to tell, from say a hundred trials, whether or not any two test chromosomes actually correspond. When we are examining non-matching chromosomes, we should get near-zero hits, allowing for “structural” stuff like centromeres.

  123. Atom,

    well said!
    Sometimes you have to make mistakes to learn something.

    So, kudos to niwrad for actually messing with the real datasets.

    I wonder, what is your conclusion to this experiment, niwrad, now that you have proven that the standard 1-2% figure is indeed a good approximation?

  124. Of related note: On this episode of ID the Future, Casey Luskin reports on a new study showing a very tangled phylogenetic tree for primates. Listen in as Luskin shows how researchers trying to create a primate phylogenetic tree are finding it isn’t as easy as they’d hoped.

    Primate Phylogenetics Challenge Darwin’s Tree of Life
    http://intelligentdesign.podom.....2_00-07_00

    ———————

    prediction: none of that will matter to neo-Darwinists!

  125. BA77, maybe you can explain the problem in your own words?

  126. What would it matter for you Indium? For no matter how contradictory the evidence is, you will blindly believe, religiously, that purely material processes are responsible for all life on earth. If I am wrong on this point please correct me and tell me exactly where you believe that Intelligent Design comes into play to explain the unrivaled complex information we find in life that no one has ever witnessed purely material processes generating.

  127. It would matter. I like to discuss these things. But I am not able to communicate with *you* when all you do is to post these links. Interacting with a wall of links is not very entertaining. Maybe you can at some point begin to think and speak for yourself!?

    So, Primate Phylogenetics! What do you think is the problem there?

  128. Indium, I think ‘the problem’ is that you, and other neo-Darwinists, refuse to concede that you have no foundation in science from which to extrapolate common descent in the first place. So what good does it do to ‘entertain’ you when you refuse to honestly address your glaring lack of a foundation in science? To put it more simply, purely material processes have never been observed to generate ANY non-trivial complex functional information whatsoever in all the history of observational science. And yet, despite this glaring lack of a foundation in science, neo-Darwinists insist that purely material processes are able to generate greater and greater heights of functional information. This is simply ludicrous to presume this.,, So thus once again Indium, what good for does it do to ‘entertain’ you about Primate Phylogenetics, or whatever, when you don’t even have a foundation in science to begin with so as to make the extrapolation of ‘bottom up’ generation of functional information from purely material processes? Frankly to ‘entertain’ someone who refuses to concede that they have no foundation in science is like arguing with someone who believes the Earth is flat.,,, Thus the Casey Luskin audio link is not listed for your benefit, or ‘entertainment’ , though I wish you would honestly consider it’s merits, but is listed priomarily for the benefit of those onlookers who have a open mind to see that neo-Darwinism falls apart upon closer inspection.,,, Moreover, I would rather concentrate on science that argue theology with you, which is what all arguments of neo-Darwinists ultimately boil down to in the end;

    Religion drives science and it matters.
    – Cornelius Hunter

    From Philosopher to Science Writer: The Dissemination of Evolutionary Thought – May 2011
    Excerpt: The powerful theory of evolution hangs on this framework of thought that mandates naturalism. The science is weak but the metaphysics are strong. This is the key to understanding evolutionary thought. The weak arguments are scientific and the strong arguments, though filled with empirical observation and scientific jargon, are metaphysical. The stronger the argument, the more theological or philosophical.
    http://darwins-god.blogspot.co.....riter.html

    Charles Darwin, Theologian: Major New Article on Darwin’s Use of Theology in the Origin of Species – May 2011
    Excerpt: “Charles Darwin’s use of theology in the Origin of Species,” BJHS 2011, argues that Darwin used theology throughout his 1859 masterwork to argue for the truth of his theory of descent with modification by natural causes. Darwin’s theology was not merely negative, entertaining the assumptions of his creationist opponents as hypotheses simply to contradict those assumptions with evidence.
    Rather, Dilley argues, Darwin employed theology in a positive fashion, as support for his own position. “In the Origin,” Dilley writes, “Darwin used a specific theological view of God’s relationship to natural laws in order to argue for evolution and against special creation.” The Origin supplies abundant evidence of theology in action; as Dilley observes
    http://www.evolutionnews.org/2.....46391.html

    ============

    This following video, at the 7:15 minute mark, is very interesting for in it you see ‘Darwinian Theology’ been played out to its fullest, and most absurd, extent.

    The Anthropic Principle – Fine Tuning Of The Universe – Michael Strauss PhD.
    http://www.metacafe.com/watch/4323661/

  129. More links, no primates!

  130. Can this method be used to distinguish a human genome from a non-human genome?

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