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Chinese Researchers Demolish Evolutionary Pseudo-Science

In recent decades the genomes of several species have been mapped out and evolutionists are using these genome data to refine their theory. They are also making some high claims. The genome data sets, say evolutionists, are adding striking new confirmations for their theory. One piece of evidence evolutionists point to is the high similarity between the human and chimpanzee genomes. The two genomes are about 95% the same and evolutionists say this shows how easily the human could have evolved from a chimp-human common ancestor. Evolution professor Dennis Venema explains:  Read more

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102 Responses to Chinese Researchers Demolish Evolutionary Pseudo-Science

  1. In fact, 6 billion years would not be enough time. The evolution of a single new protein, even by evolutionists’ incredibly optimistic assumptions, is astronomically unlikely, even given the entire age of the universe to work on the problem.

    Since the new protein nylonase evolved in less than 60 years, you are out by 8 orders of magnitude.

    That is impressive, but not a record, since Lee Strobel’s claims regarding the known precision of the cosmological constant are out by thirty orders of magnitude.

    Try harder.

    Roy

  2. Dr. Hunter, although the 99% genetically similar figure is still bandied about on the internet, even the 95% figure you quote is far too generous. Supposed genetic similarity between chimps and humans has probably been the most manipulated and abused piece of evidence that Darwinists put forth (which is really saying something considering their abuse of all the other evidence). ,,, First let’s focus on what Darwinian processes can actually explain in terms of genetic differences:

    Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012
    Excerpt: “For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be ‘neutral’). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years).
    My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be.” Doug Axe PhD.
    http://www.evolutionnews.org/2.....62351.html

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    Now to actual genetic differences. Dr. Sternberg highlights the potential for abuse here:

    Guy Walks Into a Bar and Thinks He’s a Chimpanzee: The Unbearable Lightness of Chimp-Human Genome Similarity – 2009
    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.....think.html

    In late 2011 Jeffrey P. Tomkins, using an extremely conservative approach, (and not nearly as much bias as Darwinists have) reached the figure of 87% similarity:

    Genome-Wide DNA Alignment Similarity (Identity) for 40,000 Chimpanzee DNA Sequences Queried against the Human Genome is 86–89% – Jeffrey P. Tomkins – December 28, 2011
    Excerpt: A common claim that is propagated through obfuscated research publications and popular evolutionary science authors is that the DNA of chimpanzees or chimps (Pan troglodytes) and humans (Homo sapiens) is about 98–99% similar. A major problem with nearly all past human-chimp comparative DNA studies is that data often goes through several levels of pre-screening, filtering and selection before being aligned, summarized, and discussed. Non-alignable regions are typically omitted and gaps in alignments are often discarded or obfuscated.
    In an upcoming paper, Tomkins and Bergman (2012) discuss most of the key human-chimp DNA similarity research papers on a case-by-case basis and show that the inclusion of discarded data (when provided) actually suggests a DNA similarity for humans and chimps not greater than 80–87% and quite possibly even less.
    http://www.answersingenesis.or.....n1/blastin

    Then earlier this year, 2013, with better resolution of data, and still using an extremely conservative approach (I don’t even think he included ORFan genes in his comparison), Tomkins reached the figure of 70% genetic similarity between chimps and humans:

    Comprehensive Analysis of Chimpanzee and Human Chromosomes Reveals Average DNA Similarity of 70% – by Jeffrey P. Tomkins – February 20, 2013
    Excerpt: For the chimp autosomes, the amount of optimally aligned DNA sequence provided similarities between 66 and 76%, depending on the chromosome. In general, the smaller and more gene-dense the chromosomes, the higher the DNA similarity—although there were several notable exceptions defying this trend. Only 69% of the chimpanzee X chromosome was similar to human and only 43% of the Y chromosome. Genome-wide, only 70% of the chimpanzee DNA was similar to human under the most optimal sequence-slice conditions. While, chimpanzees and humans share many localized protein-coding regions of high similarity, the overall extreme discontinuity between the two genomes defies evolutionary timescales and dogmatic presuppositions about a common ancestor.
    http://www.answersingenesis.or.....chromosome

    And though you quote the 60 ORFan gene paper DR. Hunter, the actual number of ORFan genes in humans is far higher than that figure: 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.,,, 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

    Jerry Coyne, the grand inquisitor of Darwinism himself, states that 6% of genes are ORFans:

    From Jerry Coyne, More Table-Pounding, Hand-Waving – May 2012
    Excerpt: “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.”
    Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics.
    - per ENV

    Helen Pilcher, also no friend of ID, states that up to a third of genes in each new genome sequenced are ORFan genes

    Genes from nowhere: Orphans with a surprising story – 16 January 2013 – Helen Pilcher
    Excerpt: When biologists began sequencing genomes they discovered up to a third of genes in each species seemed to have no parents or family of any kind. Nevertheless, some of these “orphan genes” are high achievers (are just as essential as ‘old’ genes),,,
    But where do they come from? With no obvious ancestry, it was as if these genes appeared out of nowhere, but that couldn’t be true. Everyone assumed that as we learned more, we would discover what had happened to their families. But we haven’t-quite the opposite, in fact.,,,
    The upshot is that the chances of random mutations turning a bit of junk DNA into a new gene seem infinitesmally small. As the French biologist Francois Jacob wrote 35 years ago, “the probability that a functional protein would appear de novo by random association of amino acids is practically zero”.,,,
    Orphan genes have since been found in every genome sequenced to date, from mosquito to man, roundworm to rat, and their numbers are still growing.
    http://ccsb.dfci.harvard.edu/w.....n_2013.pdf

    lifespy, in this following video, conservatively guessed that 20% of genes in humans are probably ORFan:

    Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – video
    http://www.youtube.com/watch?v=1Zz6vio_LhY

    Branko Kozuli PhD points out that the problem of ORFan genes is getting worse and worse for evolutionists with every new genome sequenced, with no resolution in sight:

    Proteins and Genes, Singletons and Species – Branko Kozuli PhD. Biochemistry
    Excerpt: Horizontal gene transfer is common in prokaryotes but rare in eukaryotes [89-94], so HGT cannot account for (ORFan) singletons in eukaryotic genomes, including the human genome and the genomes of other mammals.,,,
    The trend towards higher numbers of (ORFan) singletons per genome seems to coincide with a higher proportion of the eukaryotic genomes sequenced. In other words, eukaryotes generally contain a larger number of singletons than eubacteria and archaea.,,,
    That hypothesis – that evolution strives to preserve a protein domain once it stumbles upon it contradicts the power law distribution of domains. The distribution graphs clearly show that unique domains are the most abundant of all domain groups [21, 66, 67, 70, 72, 79, 82, 86, 94, 95], contrary to their expected rarity.,,,
    Evolutionary biologists of earlier generations have not anticipated [164, 165] the challenge that (ORFan) singletons pose to contemporary biologists. By discovering millions of unique genes biologists have run into brick walls similar to those hit by physicists with the discovery of quantum phenomena. The predominant viewpoint in biology has become untenable: we are witnessing a scientific revolution of unprecedented proportions.
    http://vixra.org/pdf/1105.0025v1.pdf

    So how many ORFan genes are actually in humans, nobody really knows the exact number yet. One thing is certain though, Darwinian presuppositions have been a major hindrance in elucidating the true genetic similarity/dissimilarity between humans and chimps!

  3. Roy you state that:

    “Since the new protein nylonase evolved in less than 60 years, you are out by 8 orders of magnitude.”

    Actually you better do your homework a little better:

    Why Scientists Should NOT Dismiss Intelligent Design – William Dembski
    Excerpt: “the nylonase enzyme seems “pre-designed” in the sense that the original DNA sequence was preadapted for frame-shift mutations to occur without destroying the protein-coding potential of the original gene. Indeed, this protein sequence seems designed to be specifically adaptable to novel functions.”
    http://www.uncommondescent.com.....nt-design/

    Though Darwinists love to claim this as a ‘new’ protein. The simple fact is that is the same exact enzyme/protein, esterase, with only a minor variation on its previous enzymatic activity:

    “Mutational analysis of 6-aminohexanoate-dimer hydrolase:
    Relationship between nylon oligomer hydrolytic and esterolytic activities”
    Excerpt: “Based upon the following findings, we propose that the nylon oligomer hydrolase has newly evolved through amino acid substitutions in the catalytic cleft of a pre-existing esterase with the b-lactamase-fold”.
    Taku Ohkia, Yoshiaki Wakitania, Masahiro Takeoa, Kengo Yasuhiraa, Naoki Shibatab,
    Yoshiki Higuchib, Seiji Negoroa FEBS Letters 580 (2006) 5054–5058
    http://www.uncommondescent.com.....ent-362219

  4. Nylon Eating Bacteria: NOT NEW INFORMATION – video
    http://www.youtube.com/watch?v=wkNmfA09cGg

  5. First post here, so hello world! :)

    I find the following statement interesting, from a science philosophical point of view:

    “..why humans (and other placental mammals) have a defective gene for making egg yolk in the exact spot in our genomes where chickens have the functional version of this gene..”

    I guess the question here boils down to something like the following. Is a theory which explains(*) the above observation but cannot be rejected by observations deemed scientific? BTW, I do not suggest that neo-Darwinism can explain all observations, or it has no falsifiability (so I do not take sides); but I believe this is a nice demonstration of one of the key points on which Darwinism-ID debate is based.

    (*) The word “explain” here needs further elaboration I guess. I think it may be approximately formulated as the following: Neo-Darwinian process produces a certain set of outcomes (defective gene in ALL mammals in the EXACT spot, though functional in only a subset of mammals) at a higher probability than a random process (hence, it simply says “expect the unexpected”). That’s why, I think, such an observation seems “supportive” for Darwinism. It is true that it does not predict the frequency of these certain events (therefore not a highly testable theory), nevertheless it (implicitly) suggests that the probability of the occurrence of these events is higher than what we would expect if there were no such underlying mechanism.

  6. One of my favorite bits of number juggling goes something like–

    Clouds are 98% water.
    Jellyfish are 98% water.
    So are jellyfish the same as clouds?

    It’s what’s in the 2% that matters. It’s what makes them different.

  7. What have you got to say about that, Roy? ‘Gee up, Trigger! Let’s vamoose’, is not an appropriate response.

    Your feet need to be held to the fire, since your post was so embarrassingly discredited.

  8. Though Darwinists love to claim this as a ‘new’ protein. The simple fact is that is the same exact enzyme/protein, esterase, with only a minor variation on its previous enzymatic activity:

    If you want to claim that it is not a new protein, you would do better to avoid quotes that refer to it as ‘newly evolved’. If you want to claim that it’s the same exact enzyme you’d do better to avoid citing a paper that goes into detail about how the original and new enzymes differ. And if you want to claim that the variation in activity is minor, you would do better to avoid citing a paper that states that hydrolytic activity is “significantly enhanced”. But I suppose this is the price you pay for trying to use sources that you haven’t bothered to read.

    Oh, and in case you haven’t noticed, your second extract, which describes the new enzyme in terms of amino-acid substitutions, contradicts your first extract which characterises it as a frame-shift mutation. Or maybe they’re discussing two different enzymes? Perhaps you should do your homework a little better.

    In any case, none of this has any bearing whatsoever on my point unless you can also show that the new proteins Dr Hunter is referring to differ more from their predecessors than the nylonase enzymes differ from theirs. I very much doubt you can do that.

    Roy

  9. What have you got to say about that, Roy? ‘Gee up, Trigger! Let’s vamoose’, is not an appropriate response.

    Your feet need to be held to the fire, since your post was so embarrassingly discredited.

    What planet are you on?

  10. I think there is a difference between a new protein and one that is just a small variation of a previous protein. A new protein requires the design of new DNA sequences whereas a modified protein is just a change in an existing sequence.

  11. CuriousCat @ 5: (First, welcome to UD. Fairly new here myself.)

    I find the following statement interesting. [referencing inactive egg yolk gene in placental mammals.]

    Sure this is interesting and could be evidence for evolutionary theory. But it does not preclude design – since the placental mammal doesn’t need to produce egg yolk, this gene was deactivated. The bigger question from Dr Hunter @ OP is how can evolutionary theory explain the 60 new protein-coding genes found in humans.

  12. I think there is a difference between a new protein and one that is just a small variation of a previous protein. A new protein requires the design of new DNA sequences whereas a modified protein is just a change in an existing sequence.

    But then, if current theories regarding the origins of orphan genes from transcription of mutated non-coding regions are correct, there is no such thing as a ‘new protein’.

    Roy

  13. Roy you are just embarrassing yourself now. You claimed that nylonase was a ‘new’ protein thus refuting Hunter’s claim that ORFan proteins are extremely hard to come by. But you were shown that this was merely a minor variation of a preexisting protein that was ‘designed to adapt’ (Of related note, antibiotic resistance itself is also now shown to preexist the development of antibiotics by millions of years).

    A Tale of Two Falsifications of Evolution – September 2011
    Excerpt: “Scientists were surprised at how fast bacteria developed resistance to the miracle antibiotic drugs when they were developed less than a century ago. Now scientists at McMaster University have found that resistance has been around for at least 30,000 years.”
    http://crev.info/content/11090....._evolution

    (Ancient) Cave bacteria resistant to antibiotics – April 2012
    Excerpt: Antibiotic-resistant bacteria cut off from the outside world for more than four million years have been found in a deep cave. The discovery is surprising because drug resistance is widely believed to be the result of too much treatment.,,, “Our study shows that antibiotic resistance is hard-wired into bacteria. It could be billions of years old, but we have only been trying to understand it for the last 70 years,” said Dr Gerry Wright, from McMaster University in Canada, who has analysed the microbes.
    http://www.scotsman.com/news/h.....1-2229183#

    In fact the ability to digest nylon was shown to be a repeatable adaption within 9 days for bacterial populations that are stressed/starved of other nutrients (not 60 years as you had claimed). For this to repeatably happen requires in such a short time span would require only one or two point mutations to a pre-existing protein (Axe, Gauger : Behe: Edge of Evolution).

    What are the Limits of Darwinism? A Presentation by Dr. Michael Behe at the University of Toronto – November 15th, 2012 – video
    http://www.youtube.com/watch?v=V_XN8s-zXx4

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    - Michael Behe – The Edge of Evolution – page 146

    Wheel of Fortune: New Work by Thornton’s Group Supports Time-Asymmetric Dollo’s Law – Michael Behe – October 5, 2011
    Excerpt: Darwinian selection will fit a protein to its current task as tightly as it can. In the process, it makes it extremely difficult to adapt to a new task or revert to an old task by random mutation plus selection.
    http://www.evolutionnews.org/2.....51621.html

    Following the Evidence Where It Leads: Observations on Dembski’s Exchange with Shapiro – Ann Gauger – January 2012
    Excerpt: So far, our research indicates that genuine innovation, a change to a function not already pre-existent in a protein, is beyond the reach of natural processes, even when the starting proteins are very similar in structure.
    http://www.evolutionnews.org/2.....55171.html

    This clearly is NOT a ‘new’ protein, but is merely a minor modification of a pre-existing protein! But what do you do instead of being honest when you were shown to be wrong in your claim that this is a ‘new’ protein? Why you say I have to prove that the proteins differ more than the completely unique ORFan genes/proteins that Dr. Hunter is referring to in his article? Really? That’s all? Will you stop believing in Darwinism then? Okie Dokie, let me help you with your homework then:

    The three-dimensional structure of nylon hydrolase and the mechanism of nylon-6 hydrolysis – Seiji Negoro – Dec. 2011
    SUMMARY: We performed x-ray crystallographic analyses of the 6-aminohexanoate oligomer hydrolase (NylC) from Agromyces sp. at 2.0 Å-resolution. This enzyme is a member of the N-terminal nucleophile (N-tn) hydrolase superfamily that is responsible for the degradation of the nylon-6 industry byproduct.
    We observed four identical heterodimers (27kDa+9kDa), which resulted from the autoprocessing of the precursor protein (36kDa) and which constitute the doughnut-shaped quaternary structure. The catalytic residue of NylC was identified as the N-terminal Thr267 of the 9kDa-subunit. Furthermore, each heterodimer is folded into a single domain, generating a stacked (greek symbols) core structure. Amino acid mutations at subunit interfaces of the tetramer were observed to drastically alter the thermostability of the protein. In particular, four mutations (D122G/H130/D36A/E263Q) of wild-type NylC from Arthrobacter sp. (plasmid pOAD2-encoding enzyme), with a heat denaturation temperature of T m=52°C, enhanced the protein thermostability by 36°C (T m=88° C), whereas a single mutation (G111S or L137A) decreased the stability by approximately 10°C. We examined the enzymatic hydrolysis of nylon-6 by the thermostable NylC mutant. Argon-cluster secondary ion mass spectrometry analyses of the reaction products revealed that the major peak of nylon-6 (m/z 10,000-25,000) shifted to a smaller range, producing a new peak corresponding to m/z 1500-3000 after the enzyme treatment at 60°C. In addition, smaller fragments in the soluble fraction were successively hydrolyzed to dimers and monomers. Based on these data, we propose that NylC should be designated as nylon hydrolase (or nylonase). Three potential uses of NylC for industrial and environmental applications are also discussed.
    http://www.jbc.org/content/ear.....2.full.pdf

    De Novo Origin of Human Protein-Coding Genes – 2011
    Excerpt: Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence.,,
    Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare,,,
    http://www.plosgenetics.org/ar.....en.1002379

    And as was pointed out in post 2 of this thread, that 60 number for ORFan genes/proteins is a severe underestimation:

    From Jerry Coyne, More Table-Pounding, Hand-Waving – May 2012
    Excerpt: “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.”
    Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics, cats, (and persecuting anyone who questions neo-Darwinism).
    - per ENV

    etc.. etc…

    So Roy, do you still think that Nylonase is a completely unique ‘ORFan protein’? If so I have some ocean front property in Arizona to sell you!

    Music and Verse:

    George Strait – “Ocean Front Property” – video
    https://www.youtube.com/watch?v=nNlMzNUDM8

    Romans 1:20
    For since the creation of the world His invisible attributes are clearly seen, being understood by the things that are made, even His eternal power and Godhead, so that they are without excuse,

  14. Roy:

    But then, if current theories regarding the origins of orphan genes from transcription of mutated non-coding regions are correct, there is no such thing as a ‘new protein’.

    No, Roy. If the sequence was never a protein and it then formed one, that would be a new protein.

  15. Footnote:

    Nylon Degradation – 2008
    Excerpt: At the phenotypic level, the appearance of nylon degrading bacteria would seem to involve “evolution” of new enzymes and transport systems. However, further molecular analysis of the bacterial transformation reveals mutations resulting in degeneration of pre-existing systems. The most studied of the nylon degrading bacteria is Arthrobacter sp. K172 (formerly Flavobacterium sp.70). This bacterium employs three enzymes for nylon degradation, EI (NylA), EII (NylB), and EIII (NylC), which are found on the plasmid, pOAD2.71, 72
    EI and EIII (also NylC in Agromyces sp.) have been initially characterized.73, 72 They apparently hydrolyze the cyclic forms of some nylons, which provides a linear substrate for EII. However, no detailed analysis of the mutational changes of EI or EIII has yet been performed.
    The mutational changes of EII (6-aminohexanoatedimer hydrolase) have been characterized in detail. This analysis suggests that point mutations in a carboxyesterase gene lead to amino acid substitutions in the enzyme’s catalytic cleft. This altered the enzyme’s substrate specificity sufficiently that it could also hydrolyze linear nylon oligomers.74, 75 Yet, the EII enzyme still possesses the esterase function of the parent esterase. Thus, the mutational alteration results in a reduction of the parent enzyme’s specificity (Figure 4). This enables it to hydrolyze a wider range of oligomers that include nylon oligomers.76
    Nonetheless, reduced specificity of a pre-existing enzyme is biochemically degenerative to the enzyme,77, 78 even if it provides a presumed phenotypic benefit. The “beneficial” phenotype of nylon degradation requires the a priori existence of the enzyme and its specificity. Its degeneration is not a mechanism that accounts for the origin of either the enzyme or its specificity.,,,
    http://www.answersingenesis.or.....n-bacteria

  16. The question of ORFan genes should be easy to settle, if not now, then in the near future.

    Four questions seem to be (feel free to add any more since I am just responding to this on the fly):

    1. Are these ORFan genes substantially different from other genes in the genome of the organism? Or are they just slight variations of existing elements of the genome? If they are not much different then they could be explained by various processes such as retroposons.

    Examples such as the nylonase are meaningless. There will always be small variations of current genes that may have some function but these examples cannot be used to defend naturalistic evolution since most expressed genes differ widely from each other. So resorting to such examples, is an admission that current science does not have a clue. Nobody really gives a rat’s rear end for how nylonase arose.

    2. If these ORFan genes are not slight differences from current genes then how did such genes arise? There should be a history of these types of genes progressing and then arising in genomes in various species before they become expressed. I believe the theory is that unexpressed non-functional regions of the genome mutate away till “voilá” we have a new functional gene.

    If such is the case, then other genomes all over the spectrum of animal organisms should show evidence of such genes in the process of developing into something functional.

    And for those that have already become functional by this mutation process, there should be evident in various genomes of other organisms of their non functional equivalents (that is genomic sequences that are very similar but never actually making it to a functional sequence.) This will require a lot more genomes to be sequenced but should be available in time. If such is not there, then one has to ask just how did these functional sequences arise and how were they then made functional and expressed.

    The problem with gradualistic evolution in general is that there should be forensic evidence of the paths that got the new population to the point where they are then considered a new species. This evidence should be in the populations that never made it to a new species. In other words when a new gene is formed precursors of this functional gene should be evident in the genomes of similar species. But in these related species the sequence never made it to functionality. Do we have such examples? If not then gradualistic evolution has to be abandoned because it must be there for it to be true.

    3. Just what functions do these ORFan genes have? If they are just mutated parts of a genome with no apparent meaningful function even if they are expressed, can they really be used to identify differences in genomes.

    4. How easy is it to develop a new protein by small mutations to current ones? I know Axe and Gauger say it is extremely rare but is there agreement from the scientific community with examples on how common such genes are. The fact that nylonase is offered up as an example means they do not have anything meaningful. No one would point to nylonase if there were really good examples of new gene formation. It is a classic example of the “dog barking in the night.”

  17. What nonsense is this …

    The two genomes are about 95% the same and evolutionists say this shows how easily the human could have evolved from the chimpanzee.

    No one says that ! Humans and chimpanzee are claimed to have a common ancestor not that humans evolved from the chimpanzee !

  18. LP:

    Humans and chimpanzee are claimed to have a common ancestor not that humans evolved from the chimpanzee !

    Was this alleged common ancestor chimp-like or human-like or what was it? And how can we test the claim that humans evolved from non-humans?

  19. Lincoln Phipps,

    “Humans and chimpanzee are claimed to have a common ancestor”

    and your experimental proof for this extraordinary claim is where exactly?

    http://www.uncommondescent.com.....ent-486059

  20. Lincoln Phipps:

    What nonsense is this …

    The two genomes are about 95% the same and evolutionists say this shows how easily the human could have evolved from the chimpanzee.

    No one says that ! Humans and chimpanzee are claimed to have a common ancestor not that humans evolved from the chimpanzee !

    I’m detecting the old insufferable Darwinist pomposity from Mr. Phipps. Hunter did not say that humans evolved from chimps. Read what he said carefully, Mr. Phipps. And please spare us from the condescending, smarter-than-thou outbursts. You people are not nearly as smart as you think you are.

  21. Mapou I’m sorry you have such a reading and comprehension problem but you will see that Hunter said “The two genomes are about 95% the same and evolutionists say this shows how easily the human could have evolved from the chimpanzee.”

    How about you read what he said. Carefully.

  22. bornagain77,

    That humans and chimpanzee could have a common ancestor is not an “extraordinary claim” and it is trivial to locate online (Try Wikipedia and look at the references for the Human-chimpanzee_divergence article).

    But your point is off-topic other than the burden is Cornelius Hunter’s to show where “evolutionists say this shows how easily the human could have evolved from the chimpanzee.”

    He should have said, “”evolutionists say this shows how easily the human and chimpanzee could have evolved from a common ancestor.” rather than his bizarre version.

  23. Lincoln Phipps, if I wanted literary criticism for what I read I would go to an English teacher. Since I don’t want that, I ask you once again to Please provide experimental evidence for your extraordinary claim as requested:

    “Humans and chimpanzee are claimed to have a common ancestor”

    Seeing as you are claiming knowledge about how humans, of which I am one, came to be, I have more than a few questions towards your extraordinary claim! In fact, I’ve found a number of crushing problems against your claim:

    http://www.uncommondescent.com.....ent-486059

    If you can address each point raised at the link specifically, and in order, with peer-reviewed references, I would be most appreciative of your effort! Moreover, if you choose to ignore these seemingly insurmountable problems I’ve outlined, exactly why do you believe what you claim if you have no real proof but only bald face assertion?

  24. Phipps, Hunter is a computational biologist and biophysicist and he’s well versed in the theory of evolution. If you had bothered to read his actual blog post, you would have read the next paragraph where he’s quoting Venema talking about the supposed common ancestry of human and chimps. So I’m sure you are misinterpreting what Hunter wrote.

    At any rate, some of us are tired of anal retentive Darwinists coming on this forum and acting like they’re high priests of knowledge and intelligence. You are not. The theory of evolution is not rocket science. It’s a mediocre, dime-a-dozen theory as theories go.

  25. If humans and chimps descended from a common ancestor then there are a lot of questions.

    When did this take place?

    Is there any evidence for this common ancestor other than it might explain some things?

    Where did these new species originate? Were they geographically isolated?

    How much of the changes originated after humans left Africa?

    Could the number of proteins that are different between the two species arise in the amount of time postulated? Were some of the proteins lost from the common ancestor? That is did the common ancestor possess all the genes in both humans and chimps?

    There are probably more questions to be answered and some of the questions above may be trivial or silly but they should be answerable if one is to hold that humans and chimps had a common ancestor.

  26. He should have said, “”evolutionists say this shows how easily the human and chimpanzee could have evolved from a common ancestor.” rather than his bizarre version.

    Let’s just assume that Dr. Hunter made a mistake and assume that chimps and humans have a common ancestor and Dr. Hunter will agree. Where does that lead? Any place different?

  27. Phipps:

    That humans and chimpanzee could have a common ancestor is not an “extraordinary claim” and it is trivial to locate online (Try Wikipedia and look at the references for the Human-chimpanzee_divergence article).

    It is both an extraordinary and false claim because the having a 95% genetic similarity is not a proof of common ancestry. It could just as easily be common design via genetic engineering.

  28. I just read the Wikipedia article on “Human/Chimp last common ancestor” and one expert on primates believe the ancestor was very chimp like. So Dr. Hunter’s statement may be an error or just reflect the point of view of some that humans descended from chimps.

    There does not seem to be any firm understanding based on reading the Wikipedia article.

    http://en.wikipedia.org/wiki/C.....n_ancestor

  29. Lincoln Phipps @17:

    Humans and chimpanzee are claimed to have a common ancestor not that humans evolved from the chimpanzee !

    I love how defenders of evolution get all up in arms when people talk about humans descending from chimps. “No!” they shout indignantly, “Humans and chimps descended from a common ancestor!” Completely ignoring the point in question with a quibble over wording. Yes, yes, yes, the common ancestor. Everyone knows that, but it is a mouthful to say every time.

    Humans and chimps also both descended from an amoeba — oh, not an existing amoeba, mind you, but a common ancestor creature that closely resembled an amoeba. Not from a current chimp, mind you, but from a common ancestor that probably was more similar to the chimp than the human.

    So, yes, people should speak more clearly and refer to the “common ancestor” — you know, that hypothetical evolutionary construct — rather than just saying “chimps.” But everyone knows what is meant and getting up in arms about the definition just avoids the main point. How about actually addressing the substance of Hunter’s point?

  30. Anderson @29,

    Well said.

  31. hi guys. about the egg yolk protein. acctually there is not such thing “pseudo gene ” anymore.

    second- we have a lots of evidence for parrel evolution. even on pseudogenes:

    http://www.answersingenesis.or.....3/mistakes

    so there is no evidence for evolution here.

    about to make a new protein. lets say that we whant to evolve new protein that bind 2 molecules. we need for this change 2 binding sites. a minimal binding site need 40-50 amino acid. so we need 100 amino acid. the sequence space is about 20^100. its alot

  32. the vitellogenin actually have another function:

    http://www.sciencedaily.com/re.....092428.htm

    One of these molecules is a protein called vitellogenin. “Simply put, the more vitellogenin in bees, the longer they live. Vitellogenin also guides bees to do different social tasks, such caregiving or foraging

  33. So, yes, people should speak more clearly and refer to the “common ancestor” — you know, that hypothetical evolutionary construct — rather than just saying “chimps.” But everyone knows what is meant and getting up in arms about the definition just avoids the main poin

    Unless having the wrong (linear) model makes you say stupid things, as it does in this case. Even if the 60 protein coding genes putatively found to be in humans but not chimps hold up, the generation of new genes in the human lineage isn’t the only force that can create such a pattern. When you remember chimps have been evolving for 6 million years too it’s obvious that you have to consider gene loss. That Hunter doesn’t tells you something.

    Hunter makes the same mistake in dimissing the share mutations in the egg yolk pseudogene. Oh, and mk, why is there “no such thing as a pseudogene?”. Have I missed an important proclimation?

  34. hi wd400. this is because a lots of genes consider as pseudogenes are actually not.

    but even so: : the oux pseudogene in both gorila and orang utan share stop codon at codon 107 and also a GGGATGCC duplication at codon 911 ,but both human and chimp dont have them . so this is evidence of “hot spots” in the genome according to the evolution scientist because its contradict the phylogenetic tree . but again- if we can get share mistake without commondescent, then share mistake cant prove commondescent. simple logic

  35. WD400 @ 33:

    the generation of new genes in the human lineage isn’t the only force that can create such a pattern. When you remember chimps have been evolving for 6 million years too it’s obvious that you have to consider gene loss.

    The loss of a gene or the loss of function or the loss of information is easy to observe and explain. This can be seen in the natural processes of erosion and decay. The History Channel’s Life After People (http://hft.history.com/shows/life-after-people) shows what naturally happens to designed structures without regular care and maintenance. What is amazing to me are the self-repair mechanisms that provide resistance to this natural decay in biological organisms. Do you really believe evolutionary theory adequately explains this? And of course, there is still the problem of explaining how the original functions and genes developed prior to being lost.

  36. wd400,

    “When you remember chimps have been evolving for 6 million years…”

    You are asking us to remember what happened 6 million years ago?

  37. wd400,

    What I dislike is the cherry-picking of information.

    Speculation is presented as Fact when convenient. You probably know this to be true even among various evolutionist factions. Proofs of descent based on retrovirus traces, fusion of chromosomes, gene loss (invoked only when expedient), and lots of other “Facts” that often seem to evaporate under further scrutiny. How many times have we read that the “missing link” has finally been discovered, that most of our DNA is mostly “junk,” that we have lots of “vestigial organs left over from our evolutionary journey, that our evolution is recapitulated during embryonic development, that some biological feature is “poorly designed” (really? And how well do your designs work? Oh, they don’t.), that something is a “living fossil” that somehow has defied evolution for *millions* of years of environmental changes, mutations, and natural selection, that organic tissue has miraculously survived *millions* of years of ionizing radiation that should have turned it to powder, and on and on?

    How is it that some scientists believe that humans share their common ancestor with the orangutan, and not the chimpanzee. See
    http://johngrehan.net/index.php/human-evolution/

    Where does that leave the “Facts” about our common ancestry with the chimpanzee?

    Gosh, what if all scientific publications were anonymous, and published purely on their merits and only for the sake of scientific progress? I’m not sure that this system would work (it wouldn’t), but there would certainly be a lot fewer papers!

    What if presenting and comparing new observations and findings was more important than than “winning an argument”?

    -Q

  38. Querius,

    Well, I don’t it’s evolutionary biology that has the problem with cherry picking. To take your laundry list:

    Observed patterns in ERVs and chromosomes-fusions can be best explained by common descent – so I don’t now what you mean about facts evapourating. Most (human) DNA is junk, development recapitulatoin hasn’t been part of mainstream evolutionary theory for a hundred years, living fossils evolve (and in fact, are seldom like their fossilised cousins).

    As far as I can tell precisely two scientists think the organ is the closest relative to humans. Jon grehan is a crank, who adheres to very strange school of biogeogrpahical thinking called “panbiogeography” which amounts to drawing squiggly lines on maps and calling it science. Don’t take him seriously

  39. wd400:

    Observed patterns in ERVs and chromosomes-fusions can be best explained by common descent

    Untestable claim. For one the alleged “ERVs” are just pieces and may have never been ERVs at all. And the alleged chromosome fusion had nothing to do with the alleged common ancestry.

  40. 40

    Lincoln Phipps (17):

    Thanks for pointing that out. I meant “earlier primate” and have fixed it.

  41. wd400 also asserted:

    Most (human) DNA is junk,

    Not at all. Dr. Ohno’s presupposition about what is now know as non-coding DNA are evolutionary leftovers has been shown to be incorrect. Here’s a generous description:
    http://www.news-medical.net/he.....k-DNA.aspx

    development recapitulatoin hasn’t been part of mainstream evolutionary theory for a hundred years,

    Really? Then check this out . . . the textbook is dated 2010.
    http://www.evolutionnews.org/2.....35751.html

    living fossils evolve (and in fact, are seldom like their fossilised cousins).

    Wow, that statement flies in the face of a lot of articles! Here’s an example from http://www.thecephalopodpage.org/FosCephs.php:
    “Regardless, nautiluses barely distinguishable from the ones alive today are known from the Cretaceous Period, and the subclass is by far the oldest cephalopod group, going back about half a billion years. In this sense, the living nautiluses are living fossils: animals which have changed very little over the course of around 100 million years at least.”

    As far as I can tell precisely two scientists think the organ is the closest relative to humans. Jon grehan is a crank, who adheres to very strange school of biogeogrpahical thinking called “panbiogeography” which amounts to drawing squiggly lines on maps and calling it science. Don’t take him seriously

    Great, but remember that at one time, only two scientists believed in the double helix structure of DNA, Watson and Crick. I’m not saying that the orangutan theory is correct by any means, but I don’t think “Jon Grehan is a crank” constitutes a particularly compelling rebuttal.
    http://onlinelibrary.wiley.com.....x/abstract

    -Q

  42. #40 Thank you Cornelius Hunter on that change. Obviously there is a mission-gap between us but that change is one particular bugbear cleared up.

    Regards,
    Lincoln.

  43. hi dw400.

    even with ervs there is problems:

    http://creation.com/large-scal.....troviruses

    and we even find ervs in wrong places.

  44. Querius,

    1. Ohno’s argument was no about non-coding DNA. If you read his initial presentation of the idea you’ll see how people challanged him on roles for non-coding (then mainly called spacer DNA) and how he showed the same argument applies for any sequence-specific funcational element. Although everyone here seems to have swallowed ENCODE press releases whole, it simply isn’t true that most of the genome has been revealed to have a function.

    2. The embryoes depicted in that article are not used to support recapitulation, but homology.

    3. So called living fossils evolve biochemically and at a molecular level (in fact, evolutionary change is an inevitable consequence of finite population sizes at mutation at the molecular level). Some organisms maintain ancestral morphologies (though, for instance, tuatara and coelcanths are quite derived). Why the maintanance of some body plans over millions of years is a problem for evolutionary biology I don’t know.

    4. The differnce btween Greehan and Watson and Crick is that when W&C presented their evidence everyone agreed it supported the double helix. Greehan is a crank because he continues to use a flawed method and refuses to accept the very good reasons that the scientific community has to exclude panbiogeography from science.

  45. Homology is always assumed. Asfar as the people who cry “homology” knows they are looking at homoplasy.

  46. wd400,

    1. My point wasn’t what some people now term “junk DNA,” but rather the presumption of junk in Dr. Ohno’s paper, SO MUCH “JUNK” DNA IN OUR GENOME. Yes, I’ve read his paper several times. Surely you won’t insist that Dr. Ohno differentiated between “junk” DNA and non-coding DNA.

    Why do I often get the feeling that these discussions parallel Monty Python’s dead parrot” skit or the “he’s mostly dead” dialog on Princess Bride? According to various definitions and estimates, the biochemically active fraction of DNA has increased from less than 2% to about 80%. No, we don’t know about the last 20%, but can we please not call it “junk”?

    What do you have against ENCODE? The project includes 442 scientists in 32 labs around the world. Sounds like a reasonable effort to me.

    2. Look at the photos and descriptive text of the Biology textbooks here: http://www.discovery.org/a/3935. Their point is still recapitulation giving us “important clues” about evolution—one text book points out the “gill slits” in human development. Gill slits? Really?

    3. In other words, you contend that there were spectacular changes during the half-billion (OK, the last 100 million) years of nautilus morphological stasis at a biochemical and molecular level. And where is the scientific evidence for these changes? There is none. The supposed changes are invisible. It’s simply speculation.

    4. Again, I’m NOT defending Dr. Grehan, but “he’s a crank because he continues to use a flawed method,” whether true or not, is still not a convincing scientific rebuttal. Watson and Crick had an uphill battle getting funding for their crank methods (and yes, they were crank) compared to Pauling and Corey, but remind me again, in which proceedings were Watson and Crick finally able to publish their one-page paper?

    -Q

  47. I do think Ohno new the difference between junk and non-coding. He wasn’t a fool and would have known about tRNA, rRNA. In dicussions he also made the point that a spacer element is also subject to mutational load, which was the centre of his argument. He certainly wasn’t saying “not protein therfore not functional”.

    If want to share the argument that moves from “is transcribed” to “is functional” please go ahead – I’ve yet to hear it. If you could make that argument you’d manage to get every base of every intron into the functional set…

    ENCODE is OK for what it is, a giant data dump. Much of the press that surround that dump was terrible.

  48. wd400,

    I do think Ohno new the difference between junk and non-coding.

    So why wasn’t his paper titled SO MUCH NON-CODING DNA IN OUR GENOME?

    -Q

  49. According to various definitions and estimates, the biochemically active fraction of DNA has increased from less than 2% to about 80%.

    That much, if not most, of our DNA is transcribed to RNA has been known for decades.

  50. So why wasn’t his paper titled SO MUCH NON-CODING DNA IN OUR GENOME?

    Because he was arguing most of the genome was junk, not simply non-coding.

  51. wd400,

    Because he was arguing most of the genome was junk, not simply non-coding.

    Oh really? On what page in his paper did Dr. Ohno even mention non-coding DNA or its true function? :o

    In fact, what Dr. Ohno actually wrote was

    Our view is that they are the remains of nature’s experiments which failed. The earth is strewn with fossil remains of extinct species; is it a wonder that our genome too is filled with the remains of extinct genes?

    He also speculated on some benefits of junk DNA, but my point was that Dr. Ohno made a poor assumption. A better assumption would have been that there is no “junk” in our DNA, which would be the ID assumption.

    As an intelligent scientist, Dr. Ohno made several bold predictions in his paper based on what he expected from the evolutionary process. The predictions have proved false.

    If you don’t believe me, please read his paper again.
    http://www.junkdna.com/ohno.html

    -Q

  52. goodusername @ 48 chimed in with

    That much, if not most, of our DNA is transcribed to RNA has been known for decades.

    Of course! What we’re discussing are the evolutionary assumptions in Dr. Susumu Ohno’s paper, which was written in 1972, over 40 years ago. These assumptions have, as you pointed out, been falsified.

    -Q

  53. I’ve read it. It’s amazing to me that you can read those words and get it so wrong. Nowhere in Ohno’s paper is the assumption that because a sequence in non-coding that it must be junk. Indeed, he includes regulatory elements in his set of genes, and elsewhere talks about fact spacer elements are subject to mutation too. As I say, he would also have known about functional RNAs.

    The first two paragraphs make the strongest argument for the presence of junk DNA – large variance in genome size among related groups (now shown to be correlated with effective population size and thus the strength of natural selection to remove weekly deleterious mutations) and limits on gene content set by mutational load. Ohno was wrong that most junk is the result of gene duplication. Nothing since Ohno’s time has proved him wrong about the junkiness of our genome.

  54. (perhaps you confusion stems from the fact Ohno doesn’t use the phrase non-coding? That phrase wasn’t used at the time, even though non-protein genes were well enough known).

  55. Of course! What we’re discussing are the evolutionary assumptions in Dr. Susumu Ohno’s paper, which was written in 1972, over 40 years ago. These assumptions have, as you pointed out, been falsified.

    I’m not positive, but I’m pretty sure that even in Ohno’s time it was well known that transcription wasn’t exclusive to the protein encoding region of DNA, and that there were roles for RNA other than being translated to protein. (Taking another quick look at Ohno’s 1972 paper, he doesn’t seem to clearly state one way or another, but I may be missing something.)

    But even if Ohno did believe that only the protein encoding region of DNA was transcribed, why would that be an “evolutionary assumption”? Were non-evolutionists predicting otherwise?

  56. wd400 @ 53

    Querius wrote:

    In fact, what Dr. Ohno actually wrote was

    Our view is that they are the remains of nature’s experiments which failed. The earth is strewn with fossil remains of extinct species; is it a wonder that our genome too is filled with the remains of extinct genes?

    You (wd400) responded to that part (I’m gathering):

    I’ve read it. It’s amazing to me that you can read those words and get it so wrong. Nowhere in Ohno’s paper is the assumption that because a sequence in non-coding that it must be junk.

    But if I read that excerpt Queris used, I am curious, what does the author of the paper claim are remains of “failed experiments”? And wouldn’t the author then be imply that those remains are not useful, or useful? Does the author imply those failed remains are junk or not?

    Seems pretty difficult to think that can be interpreted to mean anything but the remains are junk. So, your amazement seems to be to my amazement.

    But then again.. I’m not tracking your entire conversation. :P

  57. Ohno is saying the bits of the genome that aren’t genes are (mostly) “dead” gene duplicates. Note, he is not saying because sequences are non-coding fossils of other genes that must be junk. Indeed, he includes non-coding regulatroy sequences in his functional set. Rather, his gene duplicates idea sets out to explain what the non-functional portion of the genome (established in his earlier paragraphs/citations) must be made of and how in accumulates.

    It turns out he wasn’t entirely right. The junk sections aren’t only pseudogenes. But pseduogenes do contribute to junkiness of our genome.

  58. Looking at non-coding sections and trying to determine something is so one dimensional.

    No it can’t be that those non-coding sections are there for future considerations- like a stockroom of parts…

  59. Could it be Joe? How would you test that hypothesis?

  60. You would have to trace the genome, transcriptome, proteome, and interactome of a species for thousands of years, if not more. Meaning it will not be done anytime soon, meaning our friends here are free to speculate anything they want.
    Because here at UD you can replace observing, hypothesizing, testing, and theorizing with one step: Speculating.
    SCIENCE….

  61. wd400-

    How does one test anything wrt unguided evolution?

  62. AVS-

    Please produce testable hypotheses wrt unguided evolution or just admit that you are a clueless troll.

  63. AVS sez:

    You would have to trace the genome, transcriptome, proteome, and interactome of a species for thousands of years, if not more.

    Sounds like evolutionism to me! “Oh it takes millions of years for blah, blah, blah”

    Nice job AVS!

  64. The fact that you call it “unguided evolution” tells me everything I need to know about you. One of those things is that trying to talk to you about science would be like trying to talk to a wall.
    I would suggest that you get your science information from scientific sources, but I know that it will fall on deaf ears.

  65. Sounds like you have no idea what you are talking about, Joe.

  66. AVS:

    The fact that you call it “unguided evolution” tells me everything I need to know about you.

    So you are ignorant of what is being debated and you don’t understand what Darwin nor the modern synthesis says.

    Here’s a hint- natural selection is blind and mindless- it just eliminates the less fit (Mayr “What Evolution Is”) and the mutations, ie genetic changes are just allegedly happenstance events, ie genetic accidents.

    Therefor it is unguided evolution. OTOH there is Intelligent Design evolution- ie evolution by design- see “Not By Chance” Spetner 1997.

    That said I get my knowledge wrt evolution from sources like Darwin, Mayr, Dawkins, Gould, Shubin, Coyne, et al. They all say that evolution is unguided.

    So what, exactly, is your issue, other than ignorance?

  67. Sounds like you are just a bloviating troll, AVS.

  68. “natural selection is blind and mindless- it just eliminates the less fit”
    Do you not see the contradiction there?
    If it does any type of “singling-out” then it is not “blind.”
    You have absolutely no idea waht you are talking about. You have no knowledge to speak of on this topic, sorry.

  69. “natural selection is blind and mindless- it just eliminates the less fit”

    Do you not see the contradiction there?

    That Dawkins and Mayr for ya- Dawkins and others say NS is blind and mindless and Mayr said it just eliminates the less fit.

    Again don’t blame me for your ignorance.

  70. “Natural selection is the simple result of variation, differential reproduction, and heredity—it is mindless and mechanistic.” UCBerkley

    “Natural selection is the blind watchmaker, blind because it does not see ahead, does not plan consequences, has no purpose in view.” Dawkins in “The Blind Watchmaker”?

    Ernst Mayr in “What Evolution Is” page 281:
    On natural selection being a pressure or force

    What is meant, of course, is simply that a consistent lack of success of certain phenotypes and their elimination from the population result in the observed changes in a population

    On the role of chance:

    The first step in selection, the production of genetic variation, is almost exclusively a chance phenomenon except that the nature of the changes at a given locus is strongly constrained. Chance plays an important role even at the second step, the process of elimination of the less fit individuals. Chance may be particularly important in the haphazard survival during periods of mass extinction.

  71. SO you mash two quotes up from two unrelated people and repeat them completely out of context? You are worse than BA, at least his quotes have sources and are correctly cited to their actual individual sources.
    I’m only going to say this once more: you have no idea what you are talking about.

  72. Or:

    “Natural selection is the result of differences in survival and reproduction among individuals of a population that vary in one or more heritable traits.” Page 11 “Biology: Concepts and Applications” Starr fifth edition

  73. AVS:

    SO you mash two quotes up from two unrelated people and repeat them completely out of context?

    How are the quotes out of context? And obviously you have no idea what you are talking about

  74. So AVS gets his ignorance exposed and sez that I don’t know what I am talking about.

    Typical

  75. VERY GOOD
    See now we are learning Joe!
    I’m so proud of you.
    Notice how the definition does not use the words “blind” “mindless” or “unguided.”
    Before you start learning about science you need to learn the difference between mined quotes from your friends on here and actual information that is in context. The context is very important for many phrases, especially the ones your friends like to throw around…after they’ve taken them out of context of course.

  76. LoL!@ AVS- I have posted that quote for years. Ya see, unlike you, I know what natural selection is. And that textbook quote supports the claim that it is blind and mindless.

    Also Ernst Mayr was one of the architects of the modern synthesis. So what he has to say about it holds more weight than anyone else- or were you also ignorant of that?

    But anyway you never did support your claim that I took the quotes out of context- IOW you are an ignorant coward.

  77. AVS has falsely accused me of taking quotes out of context and mined quotes. AVS is nothing but a typical evoTARD loser.

  78. Yes completely. The person who has forgotten more biology than you will ever know is the ignorant coward here. You are totally right. Man, I wish I was as smart as you, pasting the same bullshit quote for years and years. Nice.

  79. Another evidence-free rant.

    THe fact that you didn’t understand that evolution was unguided proves your ignorance. The fact that you were ignorant of Dawkins and Mayr also proves your ignorance.

    All we have is your word that you know something. Strange you have never demonstrated any knowledge on any topic.

  80. The fact that AVS can’t supports its claim that I quoted out of context and mined quotes pretty much demonstrates the extent of AVS’ “knowledge”…

  81. You do realize that your need to validate yourself in your posts make you seem quite desperate, right?
    I’m sitting here laughing at your attempts to talk science and you’re running around with your hair on fire. Relax, everyone knows you are the sharpest marshmallow here.

  82. 82

    AVS, are you saying that Joe is wrong to characterize Darwinian evolution as “blind,” “mindless,” or “unguided”? Or are you saying that the quotes Joe used do not, in context, support the proposition that Darwinian evolution is “blind,” “mindless,” or “unguided”? Or are you saying something completely different? I am truly trying to understand your side in your exchange here with Joe, but I don’t see you actually saying anything other than to sneer at Joe. Throw me a bone here. Tell me in words adopted to the meanest understanding what exactly you point is.

  83. Thanks, Joe, for putting that pompous, bloviating troll (AVS) in its place.

  84. I’m saying that evolution has both random, or blind/mindless/unguided processes as Joe here likes to call them, as well as having non-random processes. You need both parts,and it’s the second part that you and your friends here like to ignore apparently.
    Maybe you can explain to Joe why he’s so clueless.

  85. AVS:

    Perhaps it needs to be stressed that “blind” here means non-foresighted, not controlled by a purpose or an intellect. chance variations are blind, and differential reproductive success of varieties leading to loss of the less “fit” and/or less lucky is also blind.

    Mechanical necessity, FYI, is in the sense involved, also blind. (And, if you want to claim that differential reproductive success is not reflective of random variable components, that would still obtain. But in fact, such DRS is in significant part, chance-linked.)

    And, note from the title of Dawkins’ book, The Blind Watchmaker, the sense just used comes from Darwinists.

    All of this, however, is on side tracks.

    The uniformity principle as underscored by Lyell, and as can be traced inter alia to Newton, emphasises that a proffered explanatory cause for the unobserved far past must be shown to be operating today and to be capable of relevant effects substantially similar to credible traces from the past. Otherwise, we would indeed be indulging unbridled speculation.

    A material effect and trace is functionally specific, complex organisation and associated information, and especially digitally coded functionally specific information, FSCO/I and dFSCI for short.

    These are abundant across the world of life, and lie at the core of cellular function. This, we can take it is a clear trace from the far past of origins.

    It is also quite clear that neither blind chance nor mechanical necessity nor both in concert, have been observed creating such FSCO/I and especially dFSCI. This is backed up easily by a needle in haystack analysis that shows that FSCO/I beyond 500 – 1,000 bits is well beyond the plausible blind search capacity of our solar system or the observed cosmos across 10^17 s. On grounds quite similar to those that show why the 2nd law of thermodynamics holds in statistical form.

    But we do have a knows source of such, one easily seen from even examples in this thread: foresighted, purposeful design. With billions of observed cases all around, and direct experience as to how this can be, through intelligence in action.

    On the uniformity principle, we have every good reason to infer that he best causal explanation of the similar phenomenon in life forms is also design, starting from the origin of cell based life.

    But I suppose standing by canons of proper inductive reasoning makes us into crackpots worth only contempt, name-calling and dismissal. (As you have just indulged in in threads here at UD today.)

    Well, I await your response to the UD pro-darwin essay challenge, as one who has forgotten more biology than we will ever learn. It should be quite easily done, after all it is all fact Fact FACT more certain than gravity.

    KF

  86. AVS:

    I’m saying that evolution has both random, or blind/mindless/unguided processes as Joe here likes to call them, as well as having non-random processes.

    What are these alleged non-random processes? Natural selection is blind and mindless- it doesn’t guide anything. It is a result of three processes one of which is allegedly totally random, with the other 2 having random components.

    So exactly what is it that you think that I don’t understand?

  87. I’m saying that evolution has both random, or blind/mindless/unguided processes as Joe here likes to call them…

    You mean as Dawkins and other learned and leading evolutionists call them.

    That’s the rub- I quoted the leading evos and AVS got all in a tizzy…

  88. Fine, if that’s how you want to define “blind” then be my guest. Yes there is no definite end result, but there is direction in evolution that is provided by nature. Species adapt to their environments, they change to fill ecological niches, etc.
    “loss of the less “fit” and/or less lucky is also blind”
    I disagree with that statement, it sounds completely ridiculous to me in fact. I guess that is because we have different definitions of blind.
    You see evolution as a blind man lost in a mall, I see evolution as a blind man with a white cane and a seeing-eye dog. That is the simplest way I can explain it.

  89. Natural selection guiding evolution is a hallmark of the theory. If you can’t get that through your head, Joe, then you should probably see yourself out of here before making this site look even more ridiculous.

  90. Natural selection doesn’t guide anything- that is the reality of it, AVS.

    Natural selection is blind and mindless. It lacks foresight- how can it guide anything? Where is your evidence?

  91. wd400 @ 57

    Note, he is not saying because sequences are non-coding fossils of other genes that must be junk.

    Huh?

    Dr. Ohno had some pretty good proposals based precisely on his perception that the overwhelming preponderance of human DNA was “junk” and why this might actually be important! IIRC, he estimated it at 94% at the time.

    He thought it was “junk”, called it “junk”, and hypothesized the *requirement* for a preponderance of “junk.” The title of his paper was a statement, not a question!

    However, it’s become obvious to most people that Dr. Ohno’s observations and hypotheses were “wrong”, and not that “he wasn’t entirely right.”

    -Q

  92. Ohno thought most of the genome was junk, and that prediction is supported by genomic data (again, if you disagree let me know the argument that gets form “transcribed” to “functional”). But Ohno was making a “supposition” in attemp to explain what non-coding DNA was. The extent of non-coding DNA in the genome wasn’t a emprically known fact in Ohno’s time. THis silly narrative of “we used to call it junk because we didn’t know what it did” is flat out wrong, and people that talk about junk DNA ought to know that.

  93. AVS: When may we expect a submission on the pro-darwinism essay challenge? KF

    PS: Even ignoring the random components in elimination of the less fit or less lucky through differential reproductive success, mechanical necessity is blind, non-foresighted. As in Dawkins’ Blind Watchmaker.

  94. PPS: That means, the only expressed variations that will be rewarded will be those that are immediately incrementally advantageous. And if you wish to resort to hidden (near-neutral?) chance variations in pseudo-genes or the like, they have to be coupled by happenstance to successful variations that are expressed AND so fast as they accumulate changes, so the scope of the configuration space they have to traverse successfully exponentiates, as in multiply by 4 for every additional base, here searching by chance to hit an island of function. Where 250 bases is a solar system threshold generous upper limit, i.e. 1/3 of an average protein or thereabouts. With the problem of isolated protein fold domains and singletons staring you in the face.

  95. wd400,

    But Ohno was making a “supposition” in attemp to explain what non-coding DNA was.

    No, he wasn’t. Read his paper again. He provided several very good reasons for *non-functional* DNA, not non-coding DNA.

    THis silly narrative of “we used to call it junk because we didn’t know what it did” is flat out wrong, and people that talk about junk DNA ought to know that.

    Including Dr. Ohno? Again, he called it “JUNK” in his paper.

    wd400, I’m trying to be generous and understand your point about Dr. Ohno, but your assertions make no sense to me in light of a plain reading of his paper.

    -Q

  96. I was actually trying to saying that Ohno was not making a supposition…., quoting you in 41.

    It’s good to see you have changed your mind since then and seen that Ohno was making a positive argument for the preponderance of junk DNA and not simply arguing from ignorance.

    The silly narraive, that most UDers have swalled whole, goes something like “We used to call these sequences junk DNA, just because we didn’t know what they did. Now we now it’s almost all funcational so we call it non-coding DNA”.

    That’s wrong, both because Ohno made a positive argument for junk DNA (as you now agree) and because genomic evidence shows us most of the genome is junk.

  97. Did you actually read what I wrote? You’re not getting it.

    “We used to call these sequences junk DNA, just because we didn’t know what they did. Now we now it’s almost all funcational so we call it non-coding DNA”.

    YES! Well, almost—your second sentence is garbled. Ohno called it junk for a reason. He supposed/assumed/speculated that most DNA was “junk” because he and other researchers didn’t know what it was for. Changes to this DNA didn’t seem to have any effect. Thus, it must be “junk”!

    Dr. Ohno then speculated on some possibilities why non-functional “junk” DNA might actually be beneficial, and that 94% of human DNA was the Evolutionary Junkyard of previously functional genes, in other words [drum roll] “fossil genes.”

    And Dr. Ohno was wrong.

    He would have been better off had he assumed that the DNA in question had an unknown function, that it was likely not junk. In other words, the ID paradigm.

    -Q

  98. The paper is there for anyone who wishes to read it. That you this wrong is so obvious to anyone who understands it I really don’t see any need to continue this.

  99. wd400,

    Sorry, but it’s not looking good for you. Check this out:

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

    -Q

  100. From bornagain77:

    In fact the ability to digest nylon was shown to be a repeatable adaption within 9 days for bacterial populations that are stressed/starved of other nutrients (not 60 years as you had claimed).

    But I didn’t claim that. Here is what I wrote:

    Since the new protein nylonase evolved in less than 60 years, …

    Nothing there about bacterial populations that are “stressed/starved of other nutrients”. Nothing about repeatability either. Nor was I talking about the general ability to digest nylon, but about a specific method of doing so.

    I think it’s clear that I was talking about the historical evolution of nylonase in the wild, which we have little data on the timescale of other than that it happened between the first production of nylon and the discovery of consumption by Flavobacterium circa 1975.

    Bornagain77 has conflated that with laboratory experiments involving very different circumstances (and if his twice-removed reference is to the experiments mentioned here, then also a different species and a different nylon-digestion route as well).

    But the most egregious misrepresentation bornagain77 has made is to discard the “less than” from “less than 60 years”, without which distortion his mistargeted ‘correction’ would be an obvious concoction. That he is willing to misrepresent what has been said so blatantly, when the reality can be discovered simply by moving the scroll-bar, suggests either staggering incompetence or a total disregard for the truth. Or both.

    Roy

  101. Roy, contrary to the fact that you feel slighted, I do think the distinction of less than 60 years and 9 days is fairly substantial. (funny how evolutionists get all literary when they are exposed as to having no evidence),, Regardless of your hurt feelings, the fact of the matter is that nylonase is NOT a new protein as you had claimed but is a minor variation to an existing protein that falls well within the bounds of Behe’s Edge of Evolution. Moreover, the adaptation is ‘biochemically degenerative’ to the enzyme it altered:

    Nylon Degradation – 2008
    Excerpt: At the phenotypic level, the appearance of nylon degrading bacteria would seem to involve “evolution” of new enzymes and transport systems. However, further molecular analysis of the bacterial transformation reveals mutations resulting in degeneration of pre-existing systems. The most studied of the nylon degrading bacteria is Arthrobacter sp. K172 (formerly Flavobacterium sp.70). This bacterium employs three enzymes for nylon degradation, EI (NylA), EII (NylB), and EIII (NylC), which are found on the plasmid, pOAD2.71, 72
    EI and EIII (also NylC in Agromyces sp.) have been initially characterized.73, 72 They apparently hydrolyze the cyclic forms of some nylons, which provides a linear substrate for EII. However, no detailed analysis of the mutational changes of EI or EIII has yet been performed.
    The mutational changes of EII (6-aminohexanoatedimer hydrolase) have been characterized in detail. This analysis suggests that point mutations in a carboxyesterase gene lead to amino acid substitutions in the enzyme’s catalytic cleft. This altered the enzyme’s substrate specificity sufficiently that it could also hydrolyze linear nylon oligomers.74, 75 Yet, the EII enzyme still possesses the esterase function of the parent esterase. Thus, the mutational alteration results in a reduction of the parent enzyme’s specificity (Figure 4). This enables it to hydrolyze a wider range of oligomers that include nylon oligomers.76
    Nonetheless, reduced specificity of a pre-existing enzyme is biochemically degenerative to the enzyme,77, 78 even if it provides a presumed phenotypic benefit. The “beneficial” phenotype of nylon degradation requires the a priori existence of the enzyme and its specificity. Its degeneration is not a mechanism that accounts for the origin of either the enzyme or its specificity.,,,
    http://www.answersingenesis.or.....n-bacteria

  102. A word of advise Roy, it doesn’t reflect well on you when you use Wikipedia as your primary source for evidence, as even Wikipedia itself admits:

    Wikipedia:Academic use
    Excerpt: Wikipedia is not considered a credible source. Wikipedia is increasingly used by people in the academic community, from freshman students to professors, as an easily accessible tertiary source for information about anything and everything. However, citation of Wikipedia in research papers may be considered unacceptable, because Wikipedia is not considered a credible or authoritative source.[1][2]
    This is especially true considering anyone can edit the information given at any time.
    http://en.wikipedia.org/wiki/W.....ademic_use

    Especially concerning matters on evolution and ID:

    Wikipedia’s Tyranny of the Unemployed – David Klinghoffer – June 24, 2012
    Excerpt: PLoS One has a highly technical study out of editing patterns on Wikipedia. This is of special interest to us because Wikipedia’s articles on anything to do with intelligent design are replete with errors and lies, which the online encyclopedia’s volunteer editors are vigilant about maintaining against all efforts to set the record straight.
    You simply can never outlast these folks. They have nothing better to do with their time and will always erase your attempted correction and reinstate the bogus claim, with lightning speed over and over again.
    ,,, on Wikipedia, “fact” is established by the party with the free time that’s required to wear down everyone else and exhaust them into submission. The search for truth (on wikipedia) yields to a tyranny of the unemployed.
    http://www.evolutionnews.org/2.....61281.html

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