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%!
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
Off topic, but creationist Dr. Jay Wile just posted a somewhat negative review of Eban Alexander’s book, Proof of Heaven.
We really need a forum.
Would you like to help me build a forum, invited participants mostly…
Sal
The review by Dr. Jay Wile is filled with medical errors. Wile admits his lack on study of NDE’s and it shows. As a physician who has studied NDE for 20 years and had these episodes described to me, Dr. Alexander had an NDE which was not an hallucination. Dr. Wile did not want to accept the thelogy presented by Alexander, who went into the episode with no religious belief. Dr. Wile commented from a Christian perspective. God is God to all religions, and theologies differ.
Sal, I help moderate r/creation on reddit if anyone would like to participate there.
Sal, of all the talks that you had listed of the conference this one, along with Dr. John Sanford’s, was one of the two I was most interested in watching. Will you do a synapses of the Sanford talk as well? and Do you know if a video will be made available?,,, Oh never mind, you listed the link already,,
http://creationicc.org/proceedings.php
it still is a problem for evolution to account for how the indels got fixed into a population.
I thought you knew neutral variants fixed at the mutation rate?. Of course, since indels change several bases you need many fewer events to explain the number of differences (and many of them are human-specific ERV insertions).
I wouldn’t get too excited about ORFans either…
Orphan Genes (And the peer reviewed ‘non-answer’ from Darwinists) – video
http://www.youtube.com/watch?v=1Zz6vio_LhY
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
Of Note: Branko Kozulic is on the editorial team of BioComplexity
http://bio-complexity.org/ojs/.....TeamBio/23
Moreover the ‘anomaly’ of unique ORFan genes is found in every new genome sequenced:
Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references
http://www.vimeo.com/17135166
Estimating the size of the bacterial pan-genome – Pascal Lapierre and J. Peter Gogarten – 2008
Excerpt: We have found greater than 139 000 rare (ORFan) gene families scattered throughout the bacterial genomes included in this study. The finding that the fitted exponential function approaches a plateau indicates an open pan-genome (i.e. the bacterial protein universe is of infinite size); a finding supported through extrapolation using a Kezdy-Swinbourne plot (Figure S3). This does not exclude the possibility that, with many more sampled genomes, the number of novel genes per additional genome might ultimately decline; however, our analyses and those presented in Ref. [11] do not provide any indication for such a decline and confirm earlier observations that many new protein families with few members remain to be discovered.
http://www.paulyu.org/wp-conte.....genome.pdf
At the 12:40 minute mark of the following ‘The Dictionary of Life’ video, Dr. Nelson describes the breaking point for Darwinian scenarios from the genetic evidence:
The Dictionary of Life | Origins with Dr. Paul A. Nelson – video
http://www.youtube.com/watch?f.....vCo#t=760s
The essential genome of a bacterium – 2011
Figure (C): Venn diagram of overlap between Caulobacter and E. coli ORFs (outer circles) as well as their subsets of essential ORFs (inner circles). Less than 38% of essential Caulobacter ORFs are conserved and essential in E. coli. Only essential Caulobacter ORFs present in the STING database were considered, leading to a small disparity in the total number of essential Caulobacter ORFs.
http://www.ncbi.nlm.nih.gov/pm.....201158.pdf
wd400, I saw you mention neutral variants, so as to make it seem like you were trying to be rational in all this, but perhaps it would interest you (and others) to know some of the weaknesses inherent in the ‘neutral theory’ of evolution that Darwinists are very reluctant to openly admit:
A graph featuring ‘Kimura’s Distribution’ being properly used is shown in the following video:
Further quotes on the rather embarrassing situation Darwinists now find themselves in with the ‘neutral’ theory:
At the 2:45 minute mark of the following video the mathematical roots of the junk DNA argument, that is still used by Darwinists in spite of the ENCODE findings of Sept. 2012, is traced through Haldane, Kimura, and Ohno’s work, in the 1950’s, 60’s and 70’s, in population genetics:
A bit more detail on the history of the junk DNA argument, and how it was born out of evolutionary thought, is here:
Paul Nelson had a talk at ICC 2013 on ORFans. The evolutionary paradigm hates them and thus had a predisposition to use the faulty Chimp/Human comparisons as evidence against human ORFans. Given Tomkins study, Lander’s work should be looked with suspicion.
If that is the indel mutation rate, we could test that couldn’t we and also make prediciton about the structure of the human genome. This may lead to problems.
Nevertheless, if you invoke indels as neutral, and indels are found to serve function, then we have a case where a function evolved free of selection, hance at least Dawkins is wrong if indels have some significance.
I’m curious, are evolutionists going to respond to this research or just pretend it doesn’t exist? When are the formal debates?
Can videos of these talks be viewed anywhere? Are they part of the “box sets” on the ICC page?
To my knowledge there are no videos, but supposedly audio is available. The papers are available on DVD.
Now, to save you some money, I can tell you the links I provided above will give you most of the data you would be interested in anyway.
The graphic of the indels above should give you a picture of the problem. Remove the indels, and everything looks like the evolutionary story, include them and the comparison goes down to 80-85%.
Same with the exons and introns and regulatory elements associated with the genes. Include those and the similarity of 98% is obliterated.
This has important medical significance. The regulatory regions are important. The 98% myth has de-emphasized the regulatory regions, and thus hindered the advance of medical science since the regulatory regions have influence on hereditary disease. Not good…Darwinism hurts science and medicine. Frankly, I can’t see where it has ever helped — creationist comparative anatomy and common design assumptions would have done far better than common descent assumptions as far as medicine goes, imho.
Here is a peer-reviewed paper supporting Tomkins and the functional significance of indels. It suggests indels have function, and this has impact the evolvability of humans from apes.
http://www.mobilednajournal.com/content/2/1/13
wd400:
On paper, perhaps. But no one has ever shown that to be so.
Of course YOU wouldn’t. Your position magically accomodates just about anything. Just wait until some developmental biologist demonstrates (on paper) that saltation is not only possible but the only explanation for macroevolution?
semi related:
This is the sequence of the RNA transcript encoding NADH dehydrogenase 7 in Trypanosoma brucei. What’s fascinating about this sequence is that only the nucleotides colored black in the graphic below are actually encoded in the mitochondrial DNA. The uridine nucleotides colored red have been inserted post-transcription by RNA editing. The blue asterisks (*) indicate locations where uridines have been deleted.
As you can see, almost the whole gene has been re-written post-transcription by RNA editing (without the editing, the gene is nonfunctional). Now, how would a non-intelligent process like neo-Darwinism account for this kind of phenomenon…?
http://www.facebook.com/photo......38;theater
scordova:
Ironically, it may be comparatively easier for them to be forthright about the deep past, since they only offer speculations that can be retracted and/or revised whenever needed.
It is in the present day that the accessible hard empirical facts most devastatingly impinge upon the grand story they want to tell. For example, the true extent of the differences between humans and chimps (or any other supposed closely relate species) is incompatible with their story.
What choice do they have, if they are unwilling to let go of their story and face these unwelcome facts?
For example, the true extent of the differences between humans and chimps (or any other supposed closely relate species) is incompatible with their story.
Do you want to spell out how this is the case? The indel differences between humans and chimps require far fewer mutational events to explain the the ~2% differences arising by substitution. It seems quite compatable with a 6Ma divergence time for humans and chimps.
If that is the indel mutation rate, we could test that couldn’t we and also make prediciton about the structure of the human genome. This may lead to problems.
Predict away.. but what are the problems?
Nevertheless, if you invoke indels as neutral, and indels are found to serve function, then we have a case where a function evolved free of selection, hance at least Dawkins is wrong if indels have some significance.
Lol. It’s not neutral theory or selection. It’s both. Some indels are probably selectively neutral (most of our DNA is junk, after alll) but some will be deleterious and a few might be beneficial (that’s the transposon-mediated differences in gene expression and the like).
I’m still not actually sure what the point of any of this is. DNA is an essence, the 98% figure is sacred among evolutionary biologists, it’s just what you count the number of single-nucleotide difference between the genomes.
Lol at yourself. Are you suddenly suggesting most fixed indels are the result of positive selection? Or maybe 10% or 5% or 1%. If you say 80%, then what is the evidence of that given that only about 1000 traits can be fixed via selection according to Haldane’s dilemma.
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. Don’t have a figure? Then you have no basis to Lol except at yourself since you’ll confidently assert it’s no problem for evolution yet you won’t provide figures for indel fixation rates due to selection.
Also, just because an indel’s absence might be severely deleterious does not imply positive selection was the reason they got incorporated into the population.
98% figure sacred? Sounds religious.
The number SNPs is not the only gauge of difference since phenotypic effects appear influenced by indels, or do you disagree with the above linked paper that attributes phenotypic differences to other factors than protein substitutions? Further 98% is only comparison of orthologous genes, not even the indels, introns, exons, pseudo genes, orphans, etc.
The 98% figure is misleading. I still hear bio students saying we’re 98% similar to other apes….
I obviously mean no sacred. As in it’s just a number.
What do you think an exon is? And why do you think exons introns and pseudogenes don’t have orthologues?
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 genomes
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.
I never said that, you’re attributing a claim to me I didn’t make.
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.”
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: 🙄
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:
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/f.....eb4-65.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:
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/ma.....cs2000.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? 🙂
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.
So Arlin, are humans 98% similar to chimps?
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.
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.
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.
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?
The 98% comes from looking at similar DNA sequences.
But anyway unguided evolution cannot account for exons, introns and alteranitve splicing
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?
The 98% included only “orthologous exons”.
This sentence is indeed meaningless, thanks for your editorial help and correction. The meaningful revision:
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:
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.
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.
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.
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.
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)
Link should go here http://www.annualreviews.org/d.....307.164420
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%.
http://www.uncommondescent.com.....nd-chimps/
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.
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?
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?
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)
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.
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/L.....ce_problem
Here is a sample DNA sequence in FASTA format:
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?
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.
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:
Tomkins simply devastates the fusion argument in that article.
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?
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.
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 …