Uncommon Descent Serving The Intelligent Design Community

ICC 2013: Geneticist Jeff Tomkins vs. Evolutionary Biologist who got laughed off stage

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

At the International Conference on Creationism 2013 (ICC 2013), professional geneticist Jeffrey Tomkins (along with Jerry Bergman) delivered a devastating critique of the claim that humans are 98% genetically similar to chimps. What he demonstrated was the fact that Darwinists are essentially saying “what is similar is 98% similar”, which is cherry picking. Tomkins acknowledges we are closer to chimps than daffodils, but humans are still substantially different from chimps.

I posted a less technical complaint here: With no dictionary tricks, humans only 70% similar to chimps.

Recall the “dictionary trick” whereby Tom Wolfe’s famous novel The Right Stuff can be shown to be almost 100% identical to a dictionary merely by aligning the words in Wolfe’s novel against identical words in the dictionary. The illusion of similarity is brought about by a total disregard for sentence structure and context of the words within sentences, paragraphs, and chapters. When those considerations are taken into account, it becomes preposterous to assert The Right Stuff is almost 100% identical to a dictionary. But such illegitimate lines of comparison are the staple of evolutionism.

Tomkins described the origin of the fallacious comparison as a myth that got started in reassociation kinetic methods of comparison in the mid-1970’s prior to the advent of modern sequencing techniques (like Illumina and Solexa). Reassociation kinetics was a technique where fragments of chimp and human DNA were mixed in the same chemical soup, and the DNAs that were reasonably similar would pair up, hence we got a biased sampling!

If we take genes that are found in both humans and chimps and disregard the indels, we get the 98% figure. When indels are considered, the similarity drops to 80-85%!

chimp human indel

When including other sequences, the similarity drops even further, down to 70%. But that 70% figure itself, imho, is too generous. I don’t think Tomkins used ORFans or pseudo genes or many other intergenic sequences, and he explicitly avoided the complication of Synteny. The links below go into detail. One might argue, the indels don’t have function. We don’t know that as a general rule, and even if they didn’t it still is a problem for evolution to account for how the indels got fixed into a population.

Tomkins pointed also to reports where lab workers may have contaminated the sequencing labs for Chimps with their own human DNA and thus biasing the figures! Hence re-sequencing has been done, and there is more sequencing pending to clean up these errors. He joked about the coughing and sneezing that may have gone on to cause contamination.

Further he pointed out that it seemed politically incorrect to dispute the 98% figure promoted by the reassociation kinetics work because it accorded with the false evolutionary narrative. He said, the industry is finally having to “fess up”, that some of their conclusions are “bogus”.

Tomkins has been reviewer on peer reviewed papers on genetics, he ran a genome lab at Clemson, and said if he had been the reviewer of some of the evolutionary papers he would have rejected them for publication because of the lack of clarity in their methodology, particularly in the material and methods sections of the paper.

During the answer and question session, a ranting raving evolutionary biologists gets up and whines and says something to the effect, “you’re using such inflammatory language … ‘sneeze and cough and ‘fess up’ and bogus'”. The evolutionary biologist then said, “as I said, what I have problems with is inflammatory your language, I don’t want to get into the technical details.” When he said that, he got laughed off stage. It was obvious Tomkins made an unassailable case and the evolutionary biologist didn’t want to be engage Tomkins technical assertions. Instead the evolutionary biologist grasped at irrelevant straws like Tomkins use of the words “sneeze” and “cough”. Pathetic!

Along those lines, I’ll give a sample of inflammatory language:

In science’s pecking order, evolutionary biology lurks somewhere near the bottom, far closer to phrenology than to physics

Jerry Coyne

Oh wait, that’s an evolutionist making inflammatory remarks about his own discipline, not a creationist.

I told Jeff, “I accepted the 98% figure for years, I thought it was true, creationists since Linnaeus have said we’re more similar to apes than to trees.” Jeff replied something to the effect, “that’s a good point, I accepted the 98% figure too, and I was prepared to accept it if that’s what my research indicated.” Tomkins spent 3 months reviewing the NCBI sequences himself, and Bergman devoted time to assist going through the literature. This was no small project. Tomkins lists recent peer-reviewed literature that supports his points.

Chimp/human similarity wasn’t directly a question of creation and evolution, it is a basic empirical question of the similarity in evidence today. If evolutionary biologists can’t be forthright and accurate about even basic empirical questions of data in the present day, why should they be trusted with speculations about the deep past?

NOTES:

Jeffrey Tomkins, Ph.D. (Genetics)

Jeffrey Tomkins has a Ph.D. in Genetics from Clemson University, a M.S. in Plant Science from the University of Idaho, Moscow and a B.S. in Agriculture from Washington State University. He was on the Faculty in the Dept of Genetics and Biochemistry, Clemson University, for a decade where he worked as a research technician in a plant breeding/genetics program, focusing on quantitative and physiological genetics in soybean. He is now a Staff Scientist at ICR. He has 56 publications in peer reviewed scientific journals and seven book chapters in scientific books. He is the primary author of The Design and Complexity of the Cell.

http://creation.com/dr-jeffrey-tomkins

Articles
The chromosome 2 fusion model of human evolution—part 1: re-evaluating the evidence
The chromosome 2 fusion model of human evolution—part 2: re-analysis of the genomic data
The junk DNA myth takes a well-deserved hit
Genomic monkey business—estimates of nearly identical human–chimp DNA similarity re-evaluated using omitted data

Is the human genome nearly identical to chimpanzee?—a reassessment of the literature

PS

Jerry Bergman had been an atheist while a professor before he got expelled. Thankfully he got rehired at a medical college where he has been teaching for the last 27 years.

Jerry Bergman, Ph.D., Biology

Biography

Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology at Northwest State College in Archbold OH for over 25 years. He has 9 degrees, including 7 graduate (= ‘post-graduate’ in some non-US systems) degrees. Dr Bergman is a graduate of Medical College of Ohio, Wayne State University in Detroit, The University of Toledo, and Bowling Green State University. He has over 800 publications in 12 languages and 20 books and monographs. He has also taught at the Medical College of Ohio where he was a research associate in the department of experimental pathology, and he also taught 6 years at the University of Toledo, and 7 years at Bowing Green State University.

Among his books is a monograph on peer evaluation published by the College Student Journal Press, a Fastback on the creation-evolution controversy published by Phi Delta Kappa, a book on vestigial organs with Dr George Howe (‘Vestigial Organs’ are Fully Functional), a book on psychology and religious cults, a book on religious discrimination published by Onesimus Press, and a book on mental health published by Claudius Verlag in München. He has also published a college textbook on evaluation (Boston, Houghton Mifflin Co.), and has contributed to dozens of other textbooks. He was also a consultant for over 20 science text books, mostly biology and biochemistry.

Dr Bergman has presented over one hundred scientific papers at professional and community meetings in the United States, Canada, and Europe. To discuss his research, he has been a featured speaker on many college campuses throughout the United States and Europe, and is a frequent guest on radio and television programs. His research has made the front page in newspapers throughout the country, has been featured by the Paul Harvey Show several times, and has been discussed by David Brinkley, Chuck Colson, and other nationally known commentators on national television.

His other work experience includes over ten years experience at various Mental Health/Psychology clinics as a licensed professional clinical counselor and three years full time corrections research for a large county circuit court in Michigan and inside the walls of Jackson Prison (SPSM), the largest walled prison in the world. He has also served as a consultant for CBS News, ABC News, Reader’s Digest, Amnesty International, several government agencies and for two Nobel Prize winners, including the inventor of the transistor. In the past decade he has consulted or has testified as an expert witness or consultant in almost one-hundred court cases. A Fellow of the American Scientific Association, member of The National Association for the Advancement of Science, and many other professional associations, he is listed in Who’s Who in America, Who’s Who in the Midwest and in Who’s Who in Science and Religion.

Education
M.P.H., Northwest Ohio Consortium for Public Health (Medical College of Ohio, Toledo, Ohio; University of Toledo, Toledo, Ohio; Bowling Green State University, Bowling Green, Ohio), 2001.
M.S. in biomedical science, Medical College of Ohio, Toledo, Ohio, 1999.
Ph.D. in human biology, Columbia Pacific University, San Rafael, California, 1992.
M.A. in social psychology, Bowling Green State University, Bowling Green, Ohio, 1986.
Ph.D. in measurement and evaluation, minor in psychology, Wayne State University, Detroit, Michigan, 1976.
M.Ed. in counseling and psychology, Wayne State University, Detroit, Michigan, 1971.
B.S., Wayne State University, Detroit, Michigan, 1970. Major area of study was sociology, biology, and psychology.
A.A. in Biology and Behavioral Science, Oakland Community College, Bloomfield Hills, Michigan, 1967.
http://creation.com/dr-jerry-bergman

Comments
And by the way, a literal 'diff' of two chromosomes would be enormous. Diff works on a line-by-line basis, so as soon as the first indel appears, it would throw out the alignment. That's why we use BLAST and not diff ...ThickPython
August 10, 2015
August
08
Aug
10
10
2015
07:50 PM
7
07
50
PM
PDT
And to Sal, I urge you to contact the developers of the BLAST algorithm, as you mentioned two years ago. They will tell you that there [is/was] a bug in the version that Jeff Tomkins used, and it is entirely due to this bug that he got his 70% figure. Tomkins is aware of this, but is trying to stop it from ever reaching the light of day.ThickPython
August 10, 2015
August
08
Aug
10
10
2015
04:27 PM
4
04
27
PM
PDT
The most recent fusion article from Tomkins is a disgrace. First of all he says "... in a common ancestor shared by humans and chimps, two small chromosomes somehow fused", which is completely incorrect - if a fusion occurred in the human-chimp common ancestor, then chimps would have the fusion. Then he says he expects intact telomeres in the fusion - why would he expect 5,000 - 15,000 bases of pristine telomeres? If the telomeres were intact prior to the fusion, then they would have done their job and prevented fusion in the first place. Clearly the telomeres were depleted prior to fusion. And then he expects satellite DNA at what is clearly a telomere to telomere fusion. Satellite DNA is found at centromeres, not telomeres I could go on and on ... is anyone willing to defend him?ThickPython
August 10, 2015
August
08
Aug
10
10
2015
04:25 PM
4
04
25
PM
PDT
Tomkins simply devastates the fusion argument in that article.bornagain77
August 2, 2015
August
08
Aug
2
02
2015
07:15 AM
7
07
15
AM
PDT
Here is another article/link to add to the list in the OP: http://www.icr.org/article/8830 It is entitled: "More DNA Evidence Against Human Chromosome Fusion" and gives a great run down on the problems with this favorite argument of evolutionists. Here is his conclusion:
In short, the overwhelming lack of evidence for a chromosome 2 fusion does not support the evolutionary story in any feasible way. Clearly, the so-called fusion sequence is an important functional feature called a promoter inside a highly expressed gene, not an accident of evolution.
tjguy
August 2, 2015
August
08
Aug
2
02
2015
06:54 AM
6
06
54
AM
PDT
Diff would give you a really big patch, but that’s because (as I understand it) diff doesn’t deal with rearrangements (shuffled lines).
Thanks for your comments. I eventually will have to try a few things, but I've got to start somewhere. I have contacts in the Computer Science and Bioinformatics community including those that worked on the BLAST algorithms, I might have to ping them for assistance. Thanks again.scordova
August 14, 2013
August
08
Aug
14
14
2013
09:49 PM
9
09
49
PM
PDT
Diff would give you a really big patch, but that's because (as I understand it) diff doesn't deal with rearrangements (shuffled lines).wd400
August 14, 2013
August
08
Aug
14
14
2013
09:27 PM
9
09
27
PM
PDT
You keep saying the 98% figure is fore exons only. It’s not. You are wrong about that.
So if I take chromosome 21 in human and chromosome 21 in chimp, and do an objective computerized comparison with no alignments, what do you expect? 98%? For the reader's benefit, in Configuration Management and Version Control Systems that track the versions of documents, an optimal way to track all the changes between versions is to find some sort of minimal amount of editing needed to transform one version to the other. These minimal edits are then stored in file. Thus, algorithms exist which can approximately describe the minimal number of evolutionary transformations from one string to another. The relevance of such techniques should be obvious to the question of evolving one gigantic string of DNA to another (like Chromosome 21). Such algorithms are an objective measure of the differences between strings. Hence, we ought to be able to do this between Chromosome 21 of humans and chromosome 21 of chimps if they are 98% similar. If the algorithm blows up in the attempt, this is evidence we aren't 98% similar to chimps in chromosome 21. We can then do the same for every chromosome. Any predictions as to what such an honest comparison will yield? For the reader's benefit, here is a description of this objective comparison method: http://en.wikipedia.org/wiki/Diff Lest anyone think it is illegitimate to use algorithms comparing human documents versus DNA, consider this: http://en.wikipedia.org/wiki/Longest_common_subsequence_problem
The longest common subsequence (LCS) problem is to find the longest subsequence common to all sequences in a set of sequences (often just two). Note that subsequence is different from a substring, for the terms of the former need not be consecutive. It is a classic computer science problem, the basis of file comparison programs such as diff, and has applications in bioinformatics.
Here is a sample DNA sequence in FASTA format:
gcctgaattcttttgtccactcgtgtcaggtgatttcgtaactgcaatctaagccatccagattctaagttcggatcgacgacatagctttctgtattctcgtcactcagcgcattgaaatgcactagcttgccacacattaaaatgtactacatgacacaaccagcgttgaatcgcctcttaacgctatagtaggcaacagcacggtgcgctacaggcctctcgatgatcgcctgctct tcgtagtagtaattagcccatcattttcatcccaaaggtatagacccttcacgccgtgtcttttgcctgctttcggccga
We get a file that is 48 million letters long for human chromosome 21 and one for chimp chromosome 21. Any predictions for what the diff procedure will yield?scordova
August 14, 2013
August
08
Aug
14
14
2013
08:45 PM
8
08
45
PM
PDT
Here's what I mean by dead wrong. You keep saying the 98% figure is fore exons only. It's not. You are wrong about that. BTW, that old post is classic. If I read it right, they find there is a ~0.67 chance of finding a 30 base pair run that perfectly matches between genomes. Treating each nucleotide indepentantly, that gives an expected similarity per nucleotide of 0.67^(1/30) ~ 98%! If you want a lower number just make the perfect-match criterion longer and longer you'll end up with no matches at all.wd400
August 14, 2013
August
08
Aug
14
14
2013
08:18 PM
8
08
18
PM
PDT
wd400, a bit OT but, how do the undirected processes of Darwinism write overlapping codes when I best programmers can't even do as such?
Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 - published online May 2013 Excerpt: In the last decade, we have discovered still another aspect of the multi- dimensional genome. We now know that DNA sequences are typically “ poly-functional” [38]. Trifanov previously had described at least 12 genetic codes that any given nucleotide can contribute to [39,40], and showed that a given base-pair can contribute to multiple overlapping codes simultaneously. The first evidence of overlapping protein-coding sequences in viruses caused quite a stir, but since then it has become recognized as typical. According to Kapronov et al., “it is not unusual that a single base-pair can be part of an intricate network of multiple isoforms of overlapping sense and antisense transcripts, the majority of which are unannotated” [41]. The ENCODE project [42] has confirmed that this phenomenon is ubiquitous in higher genomes, wherein a given DNA sequence routinely encodes multiple overlapping messages, meaning that a single nucleotide can contribute to two or more genetic codes. Most recently, Itzkovitz et al. analyzed protein coding regions of 700 species, and showed that virtually all forms of life have extensive overlapping information in their genomes [43]. Conclusions: Our analysis confirms mathematically what would seem intuitively obvious - multiple overlapping codes within the genome must radically change our expectations regarding the rate of beneficial mutations. As the number of overlapping codes increases, the rate of potential beneficial mutation decreases exponentially, quickly approaching zero. Therefore the new evidence for ubiquitous overlapping codes in higher genomes strongly indicates that beneficial mutations should be extremely rare. This evidence combined with increasing evidence that biological systems are highly optimized, and evidence that only relatively high-impact beneficial mutations can be effectively amplified by natural selection, lead us to conclude that mutations which are both selectable and unambiguously beneficial must be vanishingly rare. This conclusion raises serious questions. How might such vanishingly rare beneficial mutations ever be sufficient for genome building? How might genetic degeneration ever be averted, given the continuous accumulation of low impact deleterious mutations? http://www.worldscientific.com/doi/pdf/10.1142/9789814508728_0006 'It's becoming extremely problematic to explain how the genome could arise and how these multiple levels of overlapping information could arise, since our best computer programmers can't even conceive of overlapping codes. The genome dwarfs all of the computer information technology that man has developed. So I think that it is very problematic to imagine how you can achieve that through random changes in the code.,,, and there is no Junk DNA in these codes. More and More the genome looks likes a super-super set of programs.,, More and more it looks like top down design and not just bottom up chance discovery of making complex systems.' - Dr. John Sanford http://www.youtube.com/watch?feature=player_detailpage&v=YemLbrCdM_s#t=31s
Moreover wd400, besides the fact that the underlying assumptions of neo-Darwinism are now known to be false (Nobel, Shapiro) is not the gene-centric view of the genome, which you are currently defending, now overturned by the ENCODE findings of Sept. 2012?
Landscape of transcription in human cells – Sept. 6, 2012 Excerpt: Here we report evidence that three-quarters of the human genome is capable of being transcribed, as well as observations about the range and levels of expression, localization, processing fates, regulatory regions and modifications of almost all currently annotated and thousands of previously unannotated RNAs. These observations, taken together, prompt a redefinition of the concept of a gene.,,, Isoform expression by a gene does not follow a minimalistic expression strategy, resulting in a tendency for genes to express many isoforms simultaneously, with a plateau at about 10–12 expressed isoforms per gene per cell line. http://www.nature.com/nature/journal/v489/n7414/full/nature11233.html Time to Redefine the Concept of a Gene? - Sept. 10, 2012 Excerpt: As detailed in my second post on alternative splicing, there is one human gene that codes for 576 different proteins, and there is one fruit fly gene that codes for 38,016 different proteins! While the fact that a single gene can code for so many proteins is truly astounding, we didn’t really know how prevalent alternative splicing is. Are there only a few genes that participate in it, or do most genes engage in it? The ENCODE data presented in reference 2 indicates that at least 75% of all genes participate in alternative splicing. They also indicate that the number of different proteins each gene makes varies significantly, with most genes producing somewhere between 2 and 25. Based on these results, it seems clear that the RNA transcripts are the real carriers of genetic information. This is why some members of the ENCODE team are arguing that an RNA transcript, not a gene, should be considered the fundamental unit of inheritance. http://networkedblogs.com/BYdo8 Demise of the Gene - September 19, 2012 Excerpt: Although the gene has conventionally been viewed as the fundamental unit of genomic organization, on the basis of ENCODE data it is now compellingly argued that this unit is not the gene but rather the transcript (Washietl et al. 2007; Djebali et al. 2012a). On this view, genes represent a higher-order framework around which individual transcripts coalesce, creating a poly-functional entity that assumes different forms under different cellular states, guided by differential utilization of regulatory DNA. (What does our genome encode? John A. Stamatoyannopoulos Genome Res. 2012 22: 1602-1611.) http://www.evolutionnews.org/2012/09/demise_of_the_g064371.html The Extreme Complexity Of Genes - Dr. Raymond G. Bohlin - video http://www.metacafe.com/watch/8593991/
Not that the 98% myth needs to be forcefully dealt with and clearly overturned wd400, but does not all of the preceding evidence sort of make your defense of the 98% myth a bit futile and pointless? footnote: Stephen Meyer - Functional Proteins And Information For Body Plans - video http://www.metacafe.com/watch/4050681 Dr. Stephen Meyer comments at the end of the preceding video,,, ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate - 2009)bornagain77
August 14, 2013
August
08
Aug
14
14
2013
08:15 PM
8
08
15
PM
PDT
Yes, as long as you continue to be dead wrong you’ll have to justify your comments.
What do you mean me being dead wrong. Let's define what you mean by dead wrong. If I take the Y chromosome of a chimp and a human and do a DIFF (or other optimal string comparison) do you expect the Chromosomes will yield a 98% number? Of course you'll complain that's not a proper comparison, that we have to do alignments (a euphemism for a dictionary trick). How about Chromosome 21 a small one. I take a fasta file containing 48 million letters for the human. Are you saying if I do a simple Diff between the human and chimp chromosome 21, you expect that I should get 98% similarity? If you don't say that, what do you suggest -- we snip out the similar sections throw out the dissimilar sections, rearrange the sections so they line up and then compare only the similar sections (essentially a dictionary trick)? In such case, I'm not dead wrong, since you've done exactly the illegitimate comparison procedure being criticized. Maybe I could be generous, I could snip out 5 million base pair regions in the human and see if there is a corresponding 5 million base pair region at the 98% matching level. Any predictions of what I'll find? Do you want to insist I'm still dead wrong, or maybe you can define for the readers what you mean by dead wrong. Thankfully the databases are now available publicly for all to see and the net has bandwidth to download files containing 48 million characters (around 48 megabytes, likely less in compressed format). These comparisons can be done, they are not longer protected from the view of the public and filtered by the gatekeepers wishing to maintain a false narrative.scordova
August 14, 2013
August
08
Aug
14
14
2013
08:02 PM
8
08
02
PM
PDT
Sal, niwrad may be able to help with the computer stuff. He had the article a while back: 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%. https://uncommondescent.com/intelligent-design/a-simple-statistical-test-for-the-alleged-99-genetic-identity-between-humans-and-chimps/bornagain77
August 14, 2013
August
08
Aug
14
14
2013
07:59 PM
7
07
59
PM
PDT
Link should go here http://www.annualreviews.org/doi/full/10.1146/annurev.genom.9.081307.164420wd400
August 14, 2013
August
08
Aug
14
14
2013
07:13 PM
7
07
13
PM
PDT
Yes, as long as you continue to be dead wrong you'll have to justify your comments. Check out Fig. 2 here, which has percent identity in 100 kb blocks all the way along Chr2 and Chr7. Not just exons, not just genes. (and the language is Perl)wd400
August 14, 2013
August
08
Aug
14
14
2013
07:13 PM
7
07
13
PM
PDT
Wrong again. The ~98% figure includes comparisons of intergenic space, introns, regulatory elements and pseudogenes.
Good gravy, do we have to go through all this over again! Do FASTA files include intergenic sequences? JoeCoder, any computer types out there, we ought to be able to do a UNIX diff or PEARL script or whatever to these FASTA files and settle the issue. If the Synteny blows the comparison off the map we might be able to coax the comparison a bit, but we know the Chimp FASTA files are already patched according to the human genome since it wasn't done properly, so we might actually get a decent diff score. Tomkins did as much with PEARL scripts and got 70%. We can duplicate it and publish it on the net.scordova
August 14, 2013
August
08
Aug
14
14
2013
06:15 PM
6
06
15
PM
PDT
lifepsy. If the public are told that humans and chimps ar 98% alike then they aren't getting a good picture of what DNA is. If they are being told are genomes are usually about 2% different from each other then they are getting a pretty accurate picture of what our genomes look like.wd400
August 14, 2013
August
08
Aug
14
14
2013
03:37 PM
3
03
37
PM
PDT
The 98% included only “orthologous exons”. Wrong again. The ~98% figure includes comparisons of intergenic space, introns, regulatory elements and pseudogenes. ““Further 98% is only comparison of orthologous portions, not the indels, non-orthologous exons, non-orthologous pseudo genes, orphan genes (which are non-orthologous by definition), non orthologous promoter regions, non orthologous regulatory regions, non-orthologous intergenic sequences, non-orthologous large scale structures caused by synteny differences etc. Well, I guess yeah, it includes all the regions that are orthologous and not those that aren't. I don't know why'd you list them all, but fine. The point remains the "98%" accurately describes the single base pair differences between humans and chimps across most of the genome. Indels and structural variation will create more apparent divergence (i.e. more bases that don't line up between the species), but the nature of these events means we retuire fewer mutations to explain them. I don't know about a speed limit for Darwinian evolution, but Haldane's 1/300 generations is an obvious underestimate, as it assumes a population has to fix genes in serial. If Mendel's accountant found the same result we can be fairly sure that's based on false assumptions too. Even so, ~2,000 difference between humans and chimps fixed by selection seems like quite a few to me.wd400
August 14, 2013
August
08
Aug
14
14
2013
03:35 PM
3
03
35
PM
PDT
The 98% included exons, introns and pseudogenes.
The 98% included only "orthologous exons".
““Further 98% is only comparison of orthologous genes, not even the indels, introns, exons, pseudo genes, orphans, etc.””
This sentence is indeed meaningless, thanks for your editorial help and correction. The meaningful revision:
““Further 98% is only comparison of orthologous portions, not the indels, non-orthologous exons, non-orthologous pseudo genes, orphan genes (which are non-orthologous by definition), non orthologous promoter regions, non orthologous regulatory regions, non-orthologous intergenic sequences, non-orthologous large scale structures caused by synteny differences etc.
Would you agree with that? Does that make more sense. Feel free to revise it to accord with the truth. And the larger question, in light of this editorial improvement, is the 98% hypothesis improved. Heck no, Tomkins claim stands, and is probably understating if anything. Thanks for your participation and comments in my discussion. Now, if you are willing, can you answer request I posed above:
If you don’t accept Haldane’s dilemma feel free to provide for the reader the number of SNPs, indels, or whatever can be fixed via selection in 6 million years
Mendel's accountant says about 1000. Haldane's work suggest about 1000 (a figure that implicitly appears in Ohta and Kimura of 1 nucleotide substitution every 300 generation on average). Mendel's Account therefore agrees with published evolutionary literature for the last 60 years! Nothing new. If you think you have another figure feel free to provide it. As I said, I think most fixation would have to be neutral not selective.scordova
August 14, 2013
August
08
Aug
14
14
2013
09:10 AM
9
09
10
AM
PDT
wd400, for all your commenting on this article, you seem to be just focusing on minor details. I am curious what is your opinion (or any evolutionist's opinion, assuming you are one) of the substance of the research and its implications? Do you still feel the public is currently presented with an accurate picture of human-chimp genetic similarity with the ~98% claim?lifepsy
August 14, 2013
August
08
Aug
14
14
2013
04:47 AM
4
04
47
AM
PDT
The 98% comes from looking at similar DNA sequences. But anyway unguided evolution cannot account for exons, introns and alteranitve splicingJoe
August 14, 2013
August
08
Aug
14
14
2013
04:27 AM
4
04
27
AM
PDT
And just where are those fabulous proteins realized? Not necessarily just in the coding regions but exactly those regions ignored by those claiming 98% similarity between chimps and humans. This is also not true. Where do you think the 98% figure comes from?wd400
August 13, 2013
August
08
Aug
13
13
2013
10:02 PM
10
10
02
PM
PDT
Sal, if that's what you meant then this sentence is meaningless "“Further 98% is only comparison of orthologous genes, not even the indels, introns, exons, pseudo genes, orphans, etc.”" The 98% included exons, introns and pseudogenes.wd400
August 13, 2013
August
08
Aug
13
13
2013
09:50 PM
9
09
50
PM
PDT
Arlin: Can’t you people figure these things out? If you want to play scientist, you need to learn how to distinguish a bad argument from a good one.
So Arlin, are humans 98% similar to chimps?
Sequence similarity is not based on disregarding the order of nucleotides!
So disregarding indels isn't disregarding order? Heck you do worse than that! You don't just disregard order you disregard entire sets of nucleotides, you snip out words and letters to force fit a comparison. Then you disregard synteny, then non-coding regionslike the differences in promoter regions, then disregard ORFans.
Can’t you people figure these things out? If you want to play scientist, you need to learn how to distinguish a bad argument from a good one.
Actually, the problem is we figured some of the evolutionary ruses, the falsehoods and the misleading information that pretends to be science. And no, I don't want to play scientist, this is just a public blog, and it's not real science, but it does try to report on what happens in world of science. At least I'm willing to say what I write isn't real science, whereas the 98% similarity argument isn't science even though it pretends it is.scordova
August 13, 2013
August
08
Aug
13
13
2013
06:23 PM
6
06
23
PM
PDT
One of the most ambiguous of all human–chimp studies was published by Nielson et al.23 In keeping with the established obfuscational trend, only highly conserved exons were used and no data were given to allow one to calculate any type of real overall similarity. Of the total starting number of gene sequences in the analysis (20,361) the researchers decided to throw out 33% (6,630) in an ambiguously stated “very conservative quality control”. In other words, one third of the initial chimp data did not align to human, so it got tossed out. http://creation.com/human-chimp-dna-similarity-re-evaluated
scordova
August 13, 2013
August
08
Aug
13
13
2013
06:06 PM
6
06
06
PM
PDT
I should have clarified, non-orthologous non-alignable exons. I was referring to the tendency to tally only exons that are only in chimp and humans and highly alignable.scordova
August 13, 2013
August
08
Aug
13
13
2013
06:03 PM
6
06
03
PM
PDT
I wouldn’t get too excited about ORFans either…
The paper you cited by Lander is questionable even though it is a PNAS paper. Paul Nelson criticized it at ICC 2013 (more on that later) It tries to argue that human ORFans don't really exist because we don't find traces of them in dogs, or mouse. Here is science daily on Lander' "work" where lander uses the assumption of evolution to dismiss human orfans as real: :roll:
To distinguish such misidentified genes from true ones, the research team, led by Clamp and Broad Institute director Eric Lander, developed a method that takes advantage of another hallmark of protein-coding genes: conservation by evolution. 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. This evidence strengthened the case for stripping these orphans of the title, "gene."
Talk about biased distortion. They argue if the gene isn't in dogs, mice, other primates, but is found in humans, then it isn't a gene. Thus the eliminate ORFans via definition, not actually by experiment or observation of the proteins the ORFans may code for! First Jerry Coyne a few years after the Lander paper:
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. - See more at: http://www.evolutionnews.org/2012/05/from_jerry_coyn060271.html#sthash.VPDyW9rE.dpuf
Here is an example of processed pseudogene(retrogenes) that seemed to escape Lander's paper. Now that time has passed and more data emerged, the Lander paper is losing it's force. http://www.ncbi.nlm.nih.gov/pubmed/23066043 Tomkins writes on the orphan retrogenes: http://designed-dna.org/blog/files/22a6499ef684cec6339b4ab1bd610eb4-65.php But this could all be moot. Lander points out we really don't even know all the proteins we're dealing with so we're just guessing at what are and are not genes. Furthermore, the notion of "gene" is a bit misleading since alternative splicing can create lots of other protein isoforms, how many:
First, the nonredundant set of proteins has here been defined as a single representative protein from every gene locus. At present, the human genome contains 22,000–23,000 genes, although the estimated number is still changing on a monthly basis (www.ensembl.org). Thus, the nonredundant set of proteins in the human proteome is probably between 20,000 and 25,000. On the other hand, if one includes all the protein variants generated by RNA splicing or specific proteolytic processing, the number of protein isoforms rapidly increases. Splicing is a common phenomenon and frequently gives rise to different forms of the same protein, often through events linked to a targeting of the protein variants to different compartments of the cell (50). Site-specific proteolysis is particularly common in the processing of preproteins of neuropeptides, but has also been shown to be involved in the aturation of proteins, such as the cleavage of the C-peptide from the proinsulin molecule to create functional insulin and C-peptide (51). The estimated number of protein variants represented by splicing and proteolysis is still unknown, but the number might be between 50,000 and 500,000. .... Another form of variation in the human proteome is the combinatorial variants created by somatic rearrangement in cells involved in the immune system. A well-known example is the immunoglobulin G (IgG) The number of different IgG molecules in a human individual is probably more than 10 million molecules all with different complementarity-determining regions and thus different binding properties http://www.mcponline.org/content/4/4/384.full.pdf+html
And just where are those fabulous proteins realized? Not necessarily just in the coding regions but exactly those regions ignored by those claiming 98% similarity between chimps and humans. And in the case of IgG proteins, the variants are achieved via different mechanism than alternative splicing, thus the 10,000,000 IgG proteins can't easily be deduced merely looking at the DNA. From this website, http://pathmicro.med.sc.edu/mayer/iggenetics2000.htm it appears that the 10,000,000 IgG variants are sourced from only about a few hundred "genes": What if we find even more cell specific protein variants? :-)scordova
August 13, 2013
August
08
Aug
13
13
2013
05:55 PM
5
05
55
PM
PDT
What does this mean? And what is an exon? "Further 98% is only comparison of orthologous genes, not even the indels, introns, exons, pseudo genes, orphans, etc."wd400
August 13, 2013
August
08
Aug
13
13
2013
05:20 PM
5
05
20
PM
PDT
And why do you think exons introns and pseudogenes don’t have orthologues?
I never said that, you're attributing a claim to me I didn't make.scordova
August 13, 2013
August
08
Aug
13
13
2013
04:31 PM
4
04
31
PM
PDT
Raw aligned sequence similarity is a metric for similarity. Chimp, orangutan, rat, catfish, all have different degrees of raw sequence similarity to humans, and the similarity increases with other measures of genetic and evolutionary distance, including the alternative measures Tomkins suggests. If all we want to do is to ask questions like "is the chimp genome more similar, or less similar, to the human genome than the orangutan genome?", then all of these measures are going to give the same answer (more similar). This is why the raw aligned similarity measure is useful, although it may not be as good as some other measures that are harder to compute. By contrast, if we take an encyclopedia, Tom Wolfe's book, a dictionary, your local newspaper, this web page, and break them down into a word list, then ask for the overlap with dictionary words, we get 100 % every time, except for miss-spellings. Sequence similarity discriminates: vocabulary overlap with the dictionary does not. Sequence similarity is not based on disregarding the order of nucleotides! This is clear from the figure shown above. The claim of a "dictionary trick" is a false charge, whether it is coming from a geneticist or not. Can't you people figure these things out? If you want to play scientist, you need to learn how to distinguish a bad argument from a good one.arlin
August 13, 2013
August
08
Aug
13
13
2013
04:15 PM
4
04
15
PM
PDT
Jut to be clear, last 'graph of 18 should read I’m still not actually sure what the point of any of this is. DNA is not an essence, the 98% figure is not sacred among evolutionary biologists, it’s just what you get when count the number of single-nucleotide difference between the genomeswd400
August 13, 2013
August
08
Aug
13
13
2013
04:00 PM
4
04
00
PM
PDT
1 2

Leave a Reply