ID/Creationism - Comparison of Human and Chimp Genomes

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How would Creationist/ID models be used to interpret artifacts we see in species genomes? For example, looking at the human genome comparing it with chimpanzee's and the other great apes:
(1) In human chromosome 2 there is a telomere sequence and the remnants of a centromere sequence, indicating that this results from the fusion of the chimpanzee chromosomes 2p and 2q.

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I've seen the supposed fusion site and the TAG seqeunces, it seems pretty convincing. There is just one problem, there is not one but 9 pericentric inversions that total 20 million base pairs (Mb). One of them is 4 Mb long and the shortest is 2 Mb long. What is more there are inversions riddled throughout the two genomes that are not easily explained as naturally occuring.

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(2) The presence of endogenous retroviruses at the same position within the genomes of different species.

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Consider this, ERVs (actually LTRs) make up about 8% of the human genome. Do you really expect me to believe that all of this DNA is left over from germline invasions?http://www.pnas.org/...ontent-nw/full/101/suppl_2/14572/FIG1I have seen the comparisons and they generally take about half a dozen LTRs and use common alleles as markers. Then they give some convoluted estimate of them arriving independantly in the respective genomes. If we are going to talk about the Transposable Elements the first order of buisness is characterizing them, don't you?

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(3) Both chimp and humans have two 21-hydroxylase genes on their genome - a functional gene and a pseudogene. Both share the same mutation which inactivated the pseudogene.

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You see this all of the time and I am wondering if you are serious about this. This is one of those psuedo genes evolutionists want to make such a big deal about. Because there was relaxed functional constraint there was no negative selection acting on the gene so the mutation didn't kill those who had it.NCBI/eutils201 - WWW Error 404 Diagnostic

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Finally two questions on how to proceed further in Creationist/ID models:
(4) If humans and chimpanzees are supposed to be entirely separate species, how much value is there in comparing the two genomes?

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The mutation rate is 2 * 10^-8 which means that 123 germline mutations are getting passed down to the offspring. In comparing the two genomes there are no less then 145 Mb that diverge between the two genomes which leads one to wonder, how did they get there? Random mutation does not account for it so if you have some genetic basis for this I would be glad to hear about it.

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(5) In terms of ID, at what point would something be declared as 'irreducibly complex'? After such a decision, would study on such an irreducibly complex continue, and if so how? For example Michael Behe's example of the bacterial flagellum.

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How about the protein coding and regulatory genes involved with neural functions? That seems about as irreducably complex as it gets.

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As I said originally my initial post was to understand the other sides point of view, but when you put it like that...
Okay I will go with your suggestion, since I've found this area lacking in Creationist/ID literature. I also find this to be the most compelling evidence in support of evolution.

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If psuedo genes and chromosomal rearrangements are your proof then you really have your work cut out for you. The Chimpanzee Genome is now complete, would you like to share with me how many nucleotides diverge between the two perspecitve genomes? You know creationists can't be trusted to give accurate estimates, perhaps you would like to offer the details from peer reviewed scientific sources. Edited by eggasai, : Had to format a couple of thingsEdited by eggasai, : transcript errors

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Who decides wether or not they are two species?

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Species has come to mean two species that cannot interbreed. This is just a rule of thumb because the troglogytes and pygmy chimps can still interbreed but they are different enough to be considered seperate species. There is a long list of differnces from head to toe, literally, including vital organs.

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That we have concluded that they are related proves the original point and comparing for any closer resembalances is futile when we have agreed they are essentially fruits from the same tree (no pun intended)

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That's the Darwinian tree of life assumption, the problem is that it was concluded we descended from apes before biology was even a seperate discipline in science. The lineage of chimpanzees and humans going back to a common ancestor is far from confirmed. In fact the genetic distance between chimpanzees and humans is growing as we speak. Don't get me wrong, it was allways there but the old saw that the DNA is 99% the same has been proven to be false.Biological evolution makes assumptions and then makes homology arguments from any simularity. When encountering differences the explanation is allways natural selection. Adaptations are never without costs and they must be outweighed by the affects. Unless scientists have a genetic mechanism for tripling the size of an ape brain then this is all supposition and speculation about what might be an alternative to special creation.

It is an old saw, it's wrong and evolutionists know it and keep saying that 98%-99% of the Chimpanzee and human DNA is the same:"Scientists figured out decades ago that chimps are our nearest evolutionary cousins, roughly 98% to 99% identical to humans at the genetic level...But that's rapidly changing. Just a year ago, geneticists announced that they had sequenced a rough draft of the chimpanzee genome, allowing the first side-by-side comparisons of human and chimpanzee DNA."Page not found | TIMEThe paper they are refering to is the Initial Sequence of the Chimpanzee Genome (Nature, Sept 2005 available online). They did not find the DNA to be 98%-99% the same, in fact they found 35 million bases of single nucleotide substitutions, 90 Mb worth of indels and 20 Mb worth of major chromosomal rearrangements. That comes to 145 Mb in two genomes that are less then 3 billion base pairs long. That does not come to 1%-2% and the scientists that have been saying that 'for decades' have been wrong and the Science editor of Time knows that if he read the paper"Five chimpanzee bacterial artificial chromosome (BAC) sequences (described in GenBank) have been compared with the best matching regions of the human genome sequence to assay the amount and kind of DNA divergence. The conclusion is the old saw that we share 98.5% of our DNA sequence with chimpanzee is probably in error. For this sample, a better estimate would be that 95% of the base pairs are exactly shared between chimpanzee and human DNA. In this sample of 779 kb, the divergence due to base substitution is 1.4%, and there is an additional 3.4% difference due to the presence of indels."http://cat.inist.fr/?aModele=afficheN&cpsidt=13976594The ASPM gene results in a defective spindle, which in turn results in a serverly reduced brain size. Bruce Lahn, one of the authors of the paper mentioned, compared hundreds of genes involved in neural functions. He concluded that it would take hundreds if not thousands of mutations in hundreds if not thousands of genes. There is just one major problem with this, mutations affecting neural genes are exclusivly deleterious.

First of all an unnatural explanation would be mutations. If you apply the commonly held mutation rate (a mean actually) it comes to 2.5 x 10^8 which translated means 173 germline mutations per diploid generation.

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The transposable elements have been perfectly well characterized (review aricle). The interesting question is really a) why you would think that 8% of the human genome is too much, since population genetic models predict extremely high frequency of such elements under conditions such as small population size, and more importantly, b) why should humans and chimps share the SAME transposable elements? Question b is really the key here, one you failed to address.

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Notice the ERV class 1 comparisons, notice any of the comparisons. I have been looking at these ERVs for a week and I can't find a lick of substantive reasoning going into the major assumptions. I couldn't follow the link to the review but I have done some reading on the subject. For instance, the PtERV1 gene is present in Chimpanzees and OWM but is absent in Asian Great Apes and humans.

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This is one of those psuedo genes evolutionists want to make such a big deal about. Because there was relaxed functional constraint there was no negative selection acting on the gene so the mutation didn't kill those who had it.

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Relaxed functional constraint in protein coding genes or regulatory genes involved in neural functions? It does not happen, the human brian tissue has the highest physiological costs of an adaptation in the human body. Relaxed functional constraint would be deadly and what is more you are simply assuming there was a selective advantage for it.

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Since you appear to read the literature, I have to wonder whether you have done this sleight of hand on purpose. The number of point mutations is not equal to the number of nucleotide differences between two species. There are two classes of point mutation: substitution and indel (the latter is an abbreviation of insertion/deletion). A substitution involves one nucleotide being replaced with another, and results in exactly one nucleotide difference between an individual who has the mutation and an individual who does not have it. An indel, on the other hand, changes every nucleotide downstream of the mutation until a further indel puts an end to the frame shift.

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Thanks for that, it will save me having to explain this again:1) 35 million base pairs (Mb) due to single nucleotide substitutions.
2) 5 million indels, coming to 90 Mb in the respective genomes or 3%-4%.
3) 9 pericentric inversions from 2 Mb to 4 Mb in lenght, totally 20 Mb.Now that we have the biology primer out of the way we can talk about the nucleotide divergance.

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Phylogenetic and palaeontological studies suggest that humans and chimps share a most recent common ancestor around six million years ago. Generation time for chimpanzees is around 20 years. Assuming that that generation time is a reasonable approximation for the intervening primate species, and given your rate of 123 mutations per generation, we would have nearly 37 million mutations in each of the human and chimpanzee lineages in that time, i.e. a total of 74 million mutations (since there are two lineages, protochimp and protohuman, which both accumulate mutations).

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With a population of over 6 billion the human genome diverges by 1/10 of 1%, but you know what, we can get back to that one. Let's say that these are permenantly fixed, this would account for the 35 Mb worth of single nucleotide substitutions. What about the indels?

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as suggested by earlier work on portions of the chimp genome, other kinds of genomic variation turn out to be at least as important as single nucleotide base changes. Insertions and deletions have dramatically changed the landscape of the human and chimp lineages since they diverged. Duplications of sequence “contribute more genetic difference between the two species”70 megabases of material”than do single base pair substitutions,” notes Evan Eichler, also of UW, Seattle, who led a team analyzing the duplications. “It was a shocker, even to us.”

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I couldn't get your link to work but yes, these are my indels. The number of them that shocked the scientists you quoted is actually 90 Mb not 70 Mb.

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It would help to know where the 145 megabase number comes from, so we can examine your source more carefully. Could you give a reference? The results reported in the Science editorial were: 35 million single nucleotide substitions, and 5 million indels. We know that the indels gave rise to 70 megabases of divergent positions, so the authors appear to be reporting a total of 105 megabases, rather than 145, of divergent nucleotide positions caused by point mutation.

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More importantly, the total number of point mutations reported is 40 million, well within the bounds of the number of possible mutations according to your own figures.

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I thought I linked to the Chimpanzee Consortiums paper earlier but maybe not. At any rate, here is the paper and the link:Here we present a draft genome sequence of the common chimpanzee (Pan troglodytes). Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements. We use this catalogue to explore the magnitude and regional variation of mutational forces shaping these two genomes, and the strength of positive and negative selection acting on their genes. In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles. We also use the chimpanzee genome as an outgroup to investigate human population genetics and identify signatures of selective sweeps in recent human evolution.Initial sequence of the chimpanzee genome and comparison with the human genome - PubMedThe full article is available online at Nature but for some strange reason I can't get it to load. BTW, the Table above is from the same paper. Why don't you take a look and I'll check back to see what you came up with.Edited by eggasai, : No reason given.

I'm not taling about the word, I am talking about Biology as a specialized discipline. In Darwin's day they simply refered to it as naturalists. What is more I was talking about the Darwinian tree of life diagram, the only diagram in his book On the Origin of Species. Don't you people read the posts you respond to?

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So why do you think that nine pericentric inversions to be unlikely, and which genomic rearrangements do you find hard to explain through natural processes?

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Because of the nature of inversions, they do happen just like random mutations but have rare beneficial affects. For 9 of them to flip sections 2 Mb to 4 Mb in length without sever consequences is unrealistic. Particularly when inversions within human populations are so well characterized.

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Having said that, as I said in my original post, I am interested in how creationists explain the genetic evidence. As already mentioned, in the case of the human chromosome 2, we see the remnants of a second centromere region, and an additional telomere sequence. The sequence of this telomere also reverses half way though, in a head-to-head arrangement, and is flanked on either side by the same genes found on the two chimp chromosomes.

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The ERVs take up 8% of the human genome, finding a psuedo gene comparison with simular gaps is not going to be hard to do. There are simply too many assumptions here for any of this to be conclusive.Assumption 1 - The ERVs are the result of rare germline invasions resulting in 8% of the total 240 Mb of permenantly fixed DNA.Assumption 2 - Any difference in the same location and sequence identical can only be explained by a common ancestor.Assumption 3- Any ERV that shows a progressive enlarged area of divergance in succeding lines of decent are the result of mutations.The ERVs I am looking at are in psuedogenes. On the one hand if it's the same nucleotide missing in different species then it must be from common ancestor. It it's a progressive enlargement of divergance then it is a succession of mutations (why didn't the other species have mutations changing theirs I wonder). I don't buy that, for one thing I am not going to assume that a mutations account for every difference in any two genomes. Not every difference is a mutation, particularly if the gene in question just has a different amino acid there.

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Now can this evidence be described based on creationist hypotheses?

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The most important difference here is two assumptions creationists are not entangled in. One that mutations are writting and editing highly specific and precise sequences in the DNA. There are two explanations of a difference in a pseudogene in two species. One is that they were allways there and two they are vulnerable at the same site and viruses are looking for targets of opportunity.Taking a random sampling of ERVs and exaggerating their signifigance is not improving anyones understanding of genetics. It is a typical homology arguement based on anecdotal evidence. Sure a tag in a place might indicate a splice and if that were the only chromosomal rearrangement this would be a slam dunk and I would be a theistic evolutionist. When it comes to the other rearrangements all I'm getting is this rethorical question from incredulity. 'How else could this happen', or 'prove this is not the explanation', is not an argument, it's an assumption.What is infinitly more important is that you are not accounting for the divergance of humans and chimpanzees except for the Darwinian natural selection + random mutation = evolution. The fact is that mutations explain nothing except neutral affects, death, disease, disorder and an minor beneficial affect for a short space of time.Mutations do not explain anything about the 145 Mb of differences in the chimpanzee and human genomes. The mutation rate would have to be too high, there affects would be too deleterious when they had an affect and the benefits would never have been outweighed by the costs. This becomes increasingly important when you are talking about vital organs like the brain and liver, do you have any idea how conserved the protein/regulatory genes involved are? Edited by eggasai, : Typos and poorly worded statements.

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But this is mere assertion.

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We know what the creationist dogma is. You don't need to repeat it. But can you provide a shred of a scrap of a scintilla of evidence for it?

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On the contrary, the Chimpanzee Genome Project has provided considerable evidence that the DNA of chimps and humans is 3x more diverse then we have been led to believe. Just to see if you are cognizant of the issues, how much of the DNA in the genomes of chimpanzees and humans is the same?My assertions will make a lot more sense if you are aware of the actual research based on the comparison of the genomes.If you are interested in taking this to the next level take a gander at this assertion:"Pollard's analysis showed that HAR1 is essentially the same in all mammals except humans. There were only two differences between the chicken and chimp genomes in HAR1's sequence of 118 bases (bases are subunits of DNA, the As, Cs, Ts, and Gs that spell out the genetic code). This similarity means the DNA sequence remained unchanged over hundreds of millions of years of evolutionary history, an indication that it performs a biologically important function. But sometime after the human lineage diverged from its last common ancestor with chimpanzees 5 to 7 million years ago, HAR1 began to change rather dramatically."We found 18 differences between chimps and humans, which is an incredible amount of change to have happened in a few million years," Pollard said." shortened linkOne of these days evolutionists will begin to see that they grossly underestimated what would be required for apes to evolve into humans. Creationist dogma huh? Tell me something then, how does a gene that is so highly conserved for 310 million years suddenly alter 18 nucleotides in a regulatory gene 118 nucleotides long? Edited by eggasai, : rewording a statememntEdited by eggasai, : Thought I would throw in an interesting news articles.Edited by AdminJar, : No reason given.

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About 95%, according to the latest techniques. This figure will of course only be meaningful in context: for example, by seeing what the same techniques say about, for example, differences between chimps and gorillas.

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We allready know that we can expect human gene involved in brain functions to be very different then a gorilla's. The comparison of chimps and gorillas will prove very enlightning.

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You will notice that the geneticist Pollard does not conclude from this that evolution did not take place.

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No, evolution is assumed but this difference is not going to be explained by normative natural selection. You have the particulars in front of you and the chant of natural selection + mutations is going to come back and haunt you.

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... as creationists have been saying for the last century-and-a-half ...

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In that time creationism has been an intellectual and theological issue. There is the problem of decontructing Darwinism before a creationist model is possible. It will happen once people realize that there are boundries beyond which one species can transpose into an altogether different kind. Mendelian genetics is slowly providing exactly that but neither evolutionists or creationists have caught onto it yet. Creationists will have to wake up and realize that evolution is not the problem here, it's the answer. That's why evolutionists go to so much trouble to poison the well for curious creationists.

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Uh ... natural selection? Remember that?

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Selection acts if and only if a beneficial affect is produced. What is more natural selection is itself an effect, not a cause.

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I guess that's why the fossil record shows that "suddenly" (i.e. over the course of 4 million years) the cranial capacity of the lineage under question tripled.

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That must be why Homo habilis wasn't even going to be entered into the Homo catagory until they found tools in the same geological strata. He never crossed the cerebral rubicon and he was around until about 1.9 mya. With the advent of Turkana Boy and the other Homo erectus the cranial capacity jumps for less then 600cc to between 900cc and 1100cc. There are other features like the fact that Homo habilis was only about 3 foot tall and aside from bipedalism and dental work he had the body and brain of an ape. Turkana Boy, dated 1.6 mya was fully human with the exception of a cranial capacity of 900cc at full adulthood.The point is that 4 mya the cranial capacity was just over 400cc and remained static until about 2 mya. What is more you don't go changing a brian regulatory gene involved in developing the neocortex peicemeal. 18 nucleotides represent at least 6 amino acid sequences and probably more.You claim natural selection accounts for this? Fine, show be a beneficial affect from a mutation in a gene involved in neural functions. I'll save you the trouble of rummaging through the standard evolutionist propaganda because if they had an example it would be splattered all over the net.

Funny thing is the research I am reading is saying that the evolution of human brain genes is a special event.One of the study's major surprises is the relatively large number of genes that have contributed to human brain evolution. "For a long time, people have debated about the genetic underpinning of human brain evolution," said Lahn. "Is it a few mutations in a few genes, a lot of mutations in a few genes, or a lot of mutations in a lot of genes? The answer appears to be a lot of mutations in a lot of genes. We've done a rough calculation that the evolution of the human brain probably involves hundreds if not thousands of mutations in perhaps hundreds or thousands of genes -- and even that is a conservative estimate.""It is nothing short of spectacular that so many mutations in so many genes were acquired during the mere 20-25 million years of time in the evolutionary lineage leading to humans, according to Lahn. This means that selection has worked "extra-hard" during human evolution to create the powerful brain that exists in humans.Varki points out that several major events in recent human evolution may reflect the action of strong selective forces, including the appearance of the genus Homo about 2 million years ago, a major expansion of the brain beginning about a half million years ago, and the appearance of anatomically modern humans about 150,000 years ago. "It's clear that human evolution did not occur in one fell swoop," he said, "which makes sense, given that the brain is such a complex organ."Evidence that human brain evolution was a spe | EurekAlert!The first step is deconstructing Darwinism and genetics is doing a fine job of that on it's own.

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You do not suppose, do you, that the eighteen differences between us and chimps in your Gene Of The Day make us less intelligent then chimps, do you? Remember, this is a gene which usually is highly conserved.

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You really are behind in your thinking aren't you? You know what, I'm going to let you just keep wandering in circles like this. I will toss you a bone and let you know that it would have taken hundreds, if not thousands of mutations in hundreds if not thousands of genes.Let's just put it in perspective 83% of the protein coding genes show changes at an amino acid sequence level and I do mean 83% of all the protein coding genes in the human genome. There are at least 40,000 amino acids that diverge between chimps and humans, many in brian development genes.This is the clicher, you don't have 25 mya to play with or even 2.5 mya. You have the space of time from Homo habilis and Turkana Boy, that's measured in the hundreds of thousands, not millions of years.At this point it is becomeing clear that you don't even bother to read the literature. As far as I can tell you just get a few jabs and and make assinine remarks. Here's a great idea for you, when you do one of these pedantic and condescending posts of yours, have a point.

One would expect there to be a choice mutation here and there. It makes sense that certain genes are going to be different but not in genes involved in the brain or liver. However, it is exactly here that you see the spectacular mutations. Sure, 40,000 amino acids don't seem like a whole lot until you take into consideration that this is 120,000 nucleotides at the very least. Not only do they have to be substituted in triplet codons but fold into meaningfull proteins. Most of the time when an indel (mutation of length) happens a stop codon is inserted, it's just as well, it would fold into a usefull protein anyway.One of the biggest problems with most of the more dramatic mutations being in the functionally biased neural genes is the physiological costs. Even if it's an improved fittness, for say the neocortex, it still have to coordinate with the rest of the brain. Brain tissue is some of the most biologically expensive pieces of real estate in the human genome to have adaptive mutations.Then there is this regulatory gene in the Human Accelerated Region 1. Mind you, this is one of 49 and this is the most highly divergant. Turkana Boys cranium has been compared to modern Chinese and it is only slightly smaller and as far as then can tell to internal proportions are pretty close. In Homo habilis you have an ape, 3 foot tall with a cranial capacity that is very close to chimpanzees. The point being the space between Homo habilis and Tukana Boy is simply not measured in millions of years but hundreds of thousands.You do need hundreds, if not thousands of mutations in hundreds if not thousands of genes for this to happen. Like the Cambrian Explosion and every major epoch in evolution as natural history this is invariably the case. Major mophological adaptations in a relativly brief period of time. This is exactly what a creationist would expect, a sharp line of demarkation between originally created kinds.Don't take my word for genes involved with neural functions, look up mutations affecting neural functions in the human brain. There is nothing indicating beneficial affects and yet it is here that the burden of proof weighs heaviest upon the evolutionist.

How about loss of the nocicepin receptor:Typical beneficial affect, for one thing it is the loss of a receptor and the other its a phamacological effect. It inhibits two processes and produces a minor behavioral advantage. We are talking about the overhaul of a regulatory gene involved in the development of the neocortex. If we were talking about gross structural changes in a gene leading to an improved feature you might have something here. [quote]the KvB1 geneI don't know that this is a great example of a beneficial effect or not. Again form, size and complexity isn't really involved. Instead its a lack the auxiliary potassium channel. Ultimatly this is a loss of function resulting in a slight behavioral improvement.Interesting but hardly persuasive.

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Of course, the 18 mutations you described in your post are also examples, unless you consider them to have been deleterious, which is inconsistent with evidence of positive selection at the so called HAR loci.

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That's just it, these are not mutations, they are simply differences in nucleotide sequences. The only way a lineage of apes could evolve into humans is to have this alteration along with a lot of others. Remember, this is not an isolated incident, this is from one end of the genome to the other. Sure natural selection could preserve it once it happens but how does it happen is the most important question. Random mutations could not possibly pull this off, hit and miss alterations would kill the fetus in no time.

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This is certainly the standard approach of creationists, but it is not actually the first step in effecting a paradigm shift in science.

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It most certainly is because natural selection is the default explanation for absolutly everything in evolution as natural history. God is excluded a priori and the evidence becomes secondary to that.

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One would really want to forge a superior theory that can explain everything explained by evolutionary theory, plus some other things that evolutionary theory cannot explain. If all you want to do is "deconstruct Darwinism" but have not a single theory with which to replace it, that is hardly a constructive enterprise.

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Deconstructing Darwinism might well be all that is required here. Did I say that creationism was going to propel science into the 21st century and Darwinism was all that was holding them back? I don't think so, I said that deconstructing Darwinism was the first step. Then instead of a default explanation that infers either God or exclusivly naturalistic causation you simply look at what happens in living systems. Projecting into the prehistoric and primordial past is well beyond the purview of science, science is nessacarily focused on what is observed and demonstrated.

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Why not give us the Intelligent Design explanation for the origin of characteristics unique to the human brain, and let us see how it stands up against the evolutionary explanation?

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Intelligent design is simply a group of intellectuals and scientists that has said science is taking this theory beyond it's range of inquiry. It wouldn't have happened if the Darwinian didn't claim the answer for every adaptation is natural selection. It is also an a priori assumption that offers no objective standard for falsification. Show me one creationist that has a problem with Mendelian genetics, or better yet. The Human Genome Project has a website with educational material on DNA and how it works. Not once is evolution even mentioned. Biology could go on ad infinitum and never once postulate an ape man transitional and genetic researchers have yet to find a genetic basis for the evolution of the humans brain. All creationism and ID really needs is the a priori assumption removed and let the evidence do what it is supposed to, show us how living systems work.

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This thread is about the ID response to the human/chimp genome comparison, but we have heard not a single non-Darwinian hypothesis explaining the observed genome data. All we get is the standard creationist bluster, which is to claim that evolutionary theory is collapsing (just that no scientists have noticed, yet). If you have your way, and "Darwinism" is one day tossed into the grime at the back of history's fume cupboard, how are we going to explain the similarites and dissimilarities of the human and chimp genomes?

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You want to hear something ironic? If Darwinism as natural history is discarded it will be because of natural selection and how it acts on deleterious effects. I know we haven't gotten aquinted but believe me when I tell you I'm not your run of the mill creationist. In fact, I think evolution as defined scientifically is the very antithesis of the Darwinian single common ancestor model.As far as ID I think it makes some great insights into irreducible complexity. Everything in science seems to be boiling things down to an irreducible minimum, that's what is going on here. The problem is that they go the next step and say, therefore 'intellient design'. I've read Paley and I really like his analogy of a watch and a stone. it is natural theology though, that does not make it untrue or an illogical conclusion from the evidence. What it does is take the evidence outside the purview of science, into the intellectual and philosphical realms where scientists are illequiped to make an honest judgment.You want to see creationism/ID go away tommorow, drop the presumption of exclusivly naturalistic forces. Then quit pretending you know what was going on in prehistoric and primordial ages past because you don't.

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For the PtERV1 sequences (not a gene, rather a collection of genes following the basic retroviral structure of ltr-gag-pol-env-ltr) it has been found there is virtually no overlap of insertion locations between species. This suggests it is not the result of vertical transmission from a common ancestor, but instead originated from horizontal transmission (infection after the species had diverged).

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Wait a second here, if the homology arguement works in favor of common ancestor then why does the inverse logic not work. You want to focus on anecdotal evidence that favors one small segment of on ERV mutation. It's the progressive nature of the mutation that makes it so appealing a proof of common ancestry but when it is in OWM and not in humans at all you just want to dismiss it.You might want to reconsider a simple assumption. What rational reason to you have to assume that 8% of the genome is made up of the fossilized remains of viruses. These germline invasions are rare at best, the idea that hundreds of millions of base pairs of DNA are permenantly fixed in genomes by viruses is absured.

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And just to add to those numbers, the human genome is 3 billion base pairs long, and only about 1.5% of this represents protein-coding genes.

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Let me ask you this, the gorilla split with both the human and chimpanzee lineage well before the austropithicene/homo split. Would you expect that 83% of the protein coding genes would show differences at an amino acid seqeunce level? You guys like to make a priori assumptions and use anecdotal evidence but you don't like making predictions. How about the spit between western and eastern gorillas, how much would you expect two seperate species to diverge within the same genus? The gorilla/chimpanzee split goes back further then the austropithecene/homo one, how would you expect the genes to line up?Edited to add:

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Where did you get this value for the genomic divergence within the human population? Not that I doubt it, it would just be interesting to see what this was based on.

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Human Genome Projects website. It's a wonderfull place to go and look at genomics without all of this creation/evolution bluster muddying up the waters. Edited by eggasai, : No reason given.Edited by AdminJar, : No reason given.

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This is a bit of a red herring. First, natural selection is not the "default explanation for absolutely everything in evolution". In reality, neutral models of evolution are often considered to be the null hypothesis and the existence of natural selection must be inferred by departures from the predictions of that null model.

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That's not true, natural selection is not a big contributor to human evolution, it would have to be a spike in the mutation rate. They understate it but that's what the translation is, I don't think anyone is ready to explain the level of divergance."There is tentative evidence from in-depth analysis of divergence and diversity that natural selection is not the major contributor to the large-scale patterns of genetic variability in humans45, 46, 47. For these reasons, we suggest that the large-scale variation in the human-chimpanzee divergence rate primarily reflects regional variation in mutation rate." Initial sequence of the chimpanzee genome and comparison with the human genome (see genome evolution)

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If you really want to get rid of inference in biology, I'm not sure what we would be left with other than a collection of statistical descriptions of the patterns evident in nature. There would certainly be no possible causal explanation of anything. But this really does appear to be what you are suggesting

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The only inferance I want to get rid of is the a priori assumption of a single common ancestor. It has very little to do with natural selection and less then nothing to do with genomics. Evolution as scientifically defined is the change of alleles in populations over time. This need not 'infer' anything about our primordial or prehistoric past.

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First, it is a bit rich to claim that creationists or ID proponents are in some way hindered by the a priori assumptions of evolutionary biology. There is nobody stopping them from abandoning such assumptions, "simply looking at what happens in living systems" and reporting what they find. Indeed I have specifically invited you to do precisely this! hence my request for an ID explanation of the genome data.

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I have a better idea, why don't you try to elaborate on a genetic basis for the divergance between chimpanzees and humans? If there is anything more irreducibly complex it's the human brain. To date I have yet to see any of the reseach determine a viable genetic mechanism capable of pulling this off.

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I am perfectly happy to concede arguendo that evolutionary biology is a load of bunkum that cannot explain the first thing about chimpanzee genomes; that God or the divinity or intelligent agent of your choice has been monitoring and modifying the universe since its creation; and that exclusively naturalistic forces cannot explain the patterns we see in nature.

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That's how you guys get by with this, you convince creationists that they are opposed to the genuine article of science. What you really are trying to hide is the fact that your presumption of a single common ancestor has nothing to do with the actual science. Biology does not need the single common ancestor model. Mind you, I'm not saying that there are no common ancestors (plural), just that your insistance on a single common ancestor is pure undiluted mythology.

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So, let us look together at the patterns you have described:

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1. human and chimp DNA is extremely similar

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Diverging by 35 Mb of single nucleotide substitutions, 5 million indels of 90 Mb and 9 pericentric inversions from 2 Mb to 4 Mb adding up to 145 Mb. The level of divergance is simply not accounted for by the mutation rate observed in hominids. If you have a genetic mechanism for pulling this off I would love to hear about it.

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2. human DNA contains a large number of repeated units of great similarity to viral DNA

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Your talking about ERVs right? They make up 8% of the human genome and this makes for one of the all time sweeping assumptions of all time. You expect people to believe without qualification that 8% of the human genome is the fossilized remains of viruses from rare germline invasions? Your really going to have your work cut out for you on this one.

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3. the number of nonsynonymous nucleotide differences beween chimp and human DNA is smaller than the number of synonymous differences

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"The KA/KS ratio is a classical measure of the overall evolutionary constraint on a gene, where KA/KS1 indicates that a substantial proportion of amino acid changes must have been eliminated by purifying selection. Under the assumption that synonymous substitutions are neutral, KA/KS > 1 implies, but is not a necessary condition for, adaptive or positive selection. The KA/KI ratio has the same interpretation. The ratios will sometimes be denoted below by with an appropriate subscript (for example, human) to indicate the branch of the evolutionary tree under study...Given the low rate of recombination in hominid genomes (a 1 kb region experiences only 1 crossover per 100,000 generations or 2 million years), such background selection should extend beyond exons to include nearby intronic sites94. However, when the divergence rate is plotted relative to exon-intron boundaries, we find that the rate jumps sharply within a short region of 7 bp at the boundary " (Chimpanzee Genome, Nature 2005)

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Since I have dropped what you define as the a priori assumptions of biology, could you explain to me what is supposed to have become clear?

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The level of divergance, the time it had to happen in and the mutation rate. Once these are established in your mind I can explain to you what is supposed to have become clear.

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A total of 585 of the 13,454 human-chimpanzee orthologues (4.4%) have observed KA/KI > 1

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