mark kennedy v. Loudmouth: Do chimps and humans share a common ancestor?

[Loudmouth]

Do humans and apes share a common ancestor? What evidence supports this hypothesis? Even more importantly, what type of observations would be consistent with common ancestry, and which observations would be inconsistent with common ancestry?

Let’s move away from biology for just a moment. Let’s look at languages, specifically the Romance Languages (e.g., French, Spanish, Italian). These languages share a common ancestor in Vulgar Latin. When the Roman Empire fell their old territories, in which Latin was spoken, started to take on their own word usages, dialects, and finally own languages. The “evolution” of the Romance Languages looks something like this:

(source: http://en.wikipedia.org/wiki/Romance_languages ).

So how do we know that these languages are related, or rather share common ancestry? Anyone who has studied French, Spanish, or Italian will notice that some words are pronounced or spelled very similarly in each of the languages. It would seem very unlikely that two isolated cultures would independently arrive at a very similar word for the same object or action, wouldn’t it? Are not commonalities better explained by a common source than unrelated sources?

Common ancestry, through morphology and genetics, works in the same way. When we see two features that are nearly identical shared between two species it is hard to imagine that these arose independently. It is much more likely that these arose from an ancestor shared by the two species. Not only that, but the pattern of similarities should match the same tree structure that the Romance Languages fall into. This pattern is called a nested hierarchy, and it is the most powerful evidence of common ancestry. One genetic feature of primates that falls into a nested hierarchy are endogenous retroviruses (ERV’s). This will be the focus of this post.

ERV’s are retroviral genomes that have become part of the host genome. When a retrovirus attaches and injects it’s RNA into the host cell that RNA is reverse transcribed into DNA. That DNA is inserted into the host genome which then hijacks the host’s cellular processes to make more viral particles. Most of the time this occurs in somatic cells, the cells that carry out processes that keep us alive. However, once in a while a retrovirus will insert into a germ line cell which are the cells used in reproduction (ie sperm and eggs). If this insertion is somehow imperfect the virus can not replicate. The offspring produced from these germ line cells will carry a copy of retrovirus in every cell in their body. It effectively becomes part of their genome which they pass on to their offspring.

So how do we detect ERV’s in genomes? Retroviruses have very specific genes which include a reverse polymerase (pol), group specific antigen (gag), and an envelope gene (env). These genes are flanked by long terminal repeats (LTR’s) which are responsible for turning on transcription of the viral genes. Recently inserted ERV’s will have most or all of these genes. However, over time there is a high probability that the repeat regions in the flanking LTR’s will recombine with each other leaving a solo LTR in the host genome (note: repeat regions are prone to recombination).

Retroviruses insert into the host genome among many, many insertion sites. Retroviruses also have different preferences of insertion sites. For example, the table below outlines where HIV, ASLV, and MLV insert into identical human genomes. As you can see, there are thousands of insertion sites spread over the entire genome.

Caption: The human chromosomes are shown numbered. HIV integration sites from all datasets in Table 1 are shown as blue “lollipops”; MLV integration sites are shown in lavender; and ASLV integration sites are shown in green. Transcriptional activity is shown by the red shading on each of the chromosomes (derived from quantification of nonnormalized EST libraries, see text). Centromeres, which are mostly unsequenced, are shown as grey rectangles. (source: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15314653 ).

If you read the paper you will learn that these viruses prefer areas such as CpG islands and regions upstream of heavily transcribed DNA. These regions are large enough to supply thousands of possible insertion sites for each type of virus.
Much like commonalities between Romance Languages, it is exceedingly unlikely that an ERV shared at the same position in the genome between two species is due to two independent events. Therefore, if chimps and humans share an ERV at the same genomic position it is most likely that the retrovirus inserted into the genome of a common ancestor. If there are thousands of ERV’s shared in this way, it is almost certainly likely that they share a common ancestor. For this same reason, you, your parents, and your siblings share thousands of ERV’s at the same genomic position without ever being infected by a virus.
Luckily for us, both the human and chimp genomes have been sequenced. The results? Out of the ~200,000 ERV’s present in the human genome only 82 are not found in the chimp genome. In the chimp genome, only 280 can not be found in the human genome. That means that hundreds of thousands of ERV’s are shared between humans (sources: the human genome paper and the chimp genome paper referenced at the end of the post). The 360 total ERV’s that are not shared represent insertions since the chimp and human lineages diverged. This is also evidenced by the fact that these unshared ERV’s often contain env, gag, and pol genes which is consistent with a recent insertion event.
But what about the nested hierarchy that I mentioned above? If we pull back the zoom lens and look at all primates we see exactly that pattern of shared ERV’s.

Every species to the right of each arrow along the tree has those ERV’s at the same genomic position, the exact pattern that common ancestry would produce.
According to evolution there should also be another nested hierarchy created by the sequence of the shared ERV’s themselves. When two lineages diverge they will accrue mutations that are specific to that lineage. ERV’s accrue mutations just like every other piece of DNA in the genome. Using our Romance Languages analogy, each generation adds their own changes in language so that over time the languages diverge but still keep their commonalities that demonstrate their shared ancestry. The amount of time since the divergence directly correlates with the amount of difference between the languages. Therefore, if two species share a distant common ancestor there should be more sequence difference between the same shared ERV. A more recent ancestor will result in a sequence that is more alike. Therefore, a comparison of shared ERV sequences should yield the same nested hierarchy, and it does (source: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=10468595 ).

In summary, ERV’s are very strong evidence for common ancestry between chimps and humans, and for all primates for that matter. If they were not related by common ancestry we would not expect to see a nested hierarchy, the pattern that evolution and common ancestry are expected to produce. Anyone wishing to refute this argument needs to explain this fundamental observation, the presence of a nested hierarchy among shared characteristics. Not only does the genomic placement of the ERV’s produce a nested hierarchy, so does the sequence of the shared ERV’s and the same nested hierarchy at that. It is evidence like this which leads scientists to accept the hypothesis that chimps and humans share a common ancestor.

Human genome paper: http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=11237011&dopt=Abstract

Chimp genome paper: http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=16136131&dopt=Abstract

 

[mark kennedy]

In order for humans to have evolved from an ape ancestor there would have had have had a major overhaul of the most highly conserved genes in the human genome. The unprecedented expansion of the human brain in size and complexity has no known genetic basis. Specifically, What makes us human? (Chimpanzee Genome, Nature 200 ) What is the genetic basis for the threefold expansion of the human brain in 2 1/2 million years?(Human ASPM Gene, Genetics 2003) What is the genetic and evolutionary background of phenotypic traits that set humans apart from our closest evolutionary relatives, the chimpanzees?(Gene Expression Differences Between the Brain Regions, Genome Res. 2003) One of the problems with the evolutionary expansion of the human brain from that of an ape is the size, weight and complexity. The human brain would have had to triple in size, starting 2 1/2 million years ago and ending 200 to 400 thousand years ago. The brain weight would have had to grow by 250% while the body only grows by 20%. The average brain weight would have to go from 400-450g, 2 1/2 MY ago to 1350–1450 g 0.2–0.4 MY.

"It is generally believed that the brain expansion set the stage for the emergence of human language and other high-order cognitive functions and that it was caused by adaptive selection (DECAN 1992 ), yet the genetic basis of the expansion remains elusive."

Evolution of the Human ASPM Gene, a Major Determinant of Brain Size, Genetics, Vol. 165, 2063-2070, December 2003​

Researchers are unanimous in admitting that they have no clue how the most significant human trait was produced and yet insist that the case for a common ancestor has been made. What do evolutionists consider to be proof for or against the common ancestor? Apparently the Endogenous retroviruses are considered a conclusive proof but the arguments of evolutionists are riddled with flaws and misrepresentations. If you would know the truth then read what they publish, they will get it right there:

Endogenous retroviruses. Endogenous retroviruses (ERVs) have become all but extinct in the human lineage, with only a single retrovirus (human endogenous retrovirus K (HERV-K)) still active. HERV-K was found to be active in both lineages, with at least 73 human-specific insertions (7 full length and 66 solo long terminal repeats (LTRs)) and at least 45 chimpanzee-specific insertions (1 full length and 44 solo LTRs). A few other ERV classes persisted in the human genome beyond the human–chimpanzee split, leaving approx 9 human-specific insertions (all solo LTRs, including five HERV9 elements) before dying out.

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (approx5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (approx8%) to have arisen by mutation since divergence from human. It is closely related to a baboon endogenous retrovirus (BaEV, 88% ORF2 product identity) and a feline endogenous virus (ECE-1, 86% ORF2 product identity). The larger family (PtERV1) is more homogeneous and has over 200 copies. Whereas older ERVs, like HERV-K, are primarily represented by solo LTRs resulting from LTR–LTR recombination, more than half of the PtERV1 copies are still full length, probably reflecting the young age of the elements. PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

​

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). They can be found in African great apes but not in humans. What is more the ERV virus is nearly extinct in the human genome with only a couple that actually work. The only thing that ERVs are proof of is the lengths evolutionists will go to to conflate and confuse the evidence.

For almost half a century it was believed that Chimpanzee and Human DNA was virtually identical. This is now known to be false. The Comparison of Human Chromosome 21 and Chimpanzee Chromosome 22 revealed that 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level. These included gross structural changes affecting gene products far more common than previously estimated (20.3% of the PTR22 proteins) (Nature, 27 May 2004). Genome wide the differences are now known to include 35 million single base substitutions, and five million indels (with the ~70,000 indels larger than 80 bp comprising 73% of the affected base pairs). This is in addition to 8 chromosomal rearrangements from 2 million base pairs to 4 million base pairs in length coming to more then 20 million base pairs.

When you compare these differences to the known mutation rates this simply does not add up. My opponent has went on record as saying:

Out of the ~200,000 ERV’s present in the human genome only 82 are not found in the chimp genome. In the chimp genome, only 280 can not be found in the human genome. That means that hundreds of thousands of ERV’s are shared between humans (sources: the human genome paper and the chimp genome paper referenced at the end of the post). The 360 total ERV’s that are not shared represent insertions since the chimp and human lineages diverged

I am going to put the facts on the table and dispense with this claim in later rounds. The evidence against a common ancestor for chimpanzees and humans is overwhelming. The truth is slowly coming out, the differences are far greater then evolutionists have been telling us:

Gene families are groups of homologous genes that are likely to have highly similar functions. Differences in family size due to lineage-specific gene duplication and gene loss may provide clues to the evolutionary forces that have shaped mammalian genomes. Here we analyze the gene families contained within the whole genomes of human, chimpanzee, mouse, rat, and dog. In total we find that more than half of the 9,990 families present in the mammalian common ancestor have either expanded or contracted along at least one lineage. Additionally, we find that a large number of families are completely lost from one or more mammalian genomes, and a similar number of gene families have arisen subsequent to the mammalian common ancestor. Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives.

Introduction
Explaining the obvious morphological, physiological, and behavioral traits that separate modern humans from our closest relatives, the chimpanzees, is challenging given the low level of nucleotide divergence between the two species [1]. More than 30 years have passed since King and Wilson first pointed out this apparent paradox, saying that “the genetic distance between humans and the chimpanzee is probably too small to account for their substantial organismal differences” [2]. To explain the paradox, King and Wilson proposed that regulatory changes rather than protein-coding mutations were responsible for the vast majority of observed biological differences [2]. Evidence gathered since that time demonstrates that amino acid [e.g. refs.1], [3], [4], [5] and regulatory sequence [6], [7] changes have both been involved in the evolution of uniquely human phenotypes.
​

The Evolution of Mammalian Gene Families

The problem is simple enough, since our common ancestor there would have had to be 35 million single base substitutions. That comes to 140 per diploid generation for 5 million years. That is in addition to 1 indel 14 base pairs long per year for the same amount of time and the vast majority of these would have to be fixed.

Instead of demonstrating how this is remotely possible given the known mutation rate evolutionists would rather talk about this: Phylogenies of seven HERV loci. When 8% of the human genome is made up of ERVs with a 94% nucleotide sequence identity should we really be supprised the seven loci are the same? For HERV-K JML 6.17 they identified 5 substitutions, a couple of them had as many as 10. This is supposed to be some kind of proof?

Here they discuss the probability of the 11 substitutions, assuming they happened by chance:

Although it is possible that any one position may suffer an identical substitution in both LTRs by chance, the probability of 11 positions undergoing identical substitutions in both LTRs is exceedingly low.

My question would be this: with a mutation rate of 2.3 x 10^-9 for length mutations what are the odds 1 indel, 14 base pairs in length fixed every year for 5 million years? That is in addition to the 6 single base pairs substituted per year in the same time frame.

 

[Loudmouth]

This is a rebuttal of my opponents opening argument.

Brain size

mark kennedy (MK hereafter) argues that scientists do not know the specific genetic basis for human brain development. He is right. So what? How does this demonstrate that we do not share a common ancestor with chimps? MK doesn't say.

Does MK, or any scientist for that matter, think that the difference between human and chimp brainsize is due to something other than a difference DNA sequence? While scientists may not know the SPECIFIC mechanism, I think there is really zero doubt the explanation is mutations that arose in the human lineage since the chimp and human lineages diverged. If MK has evidence otherwise I would be glad to see it.

Mutation Rates

MK has argued that the difference between the human and chimp genomes is too large to be explained by 5 million years of mutations. I can't find a single reference to any study or calculations that shows this to be true. Not a single one. Even worse, after MK states that the difference is impossible he asks me to do the calculations. You would think that someone who claims something is impossible would have already done those calculations.

Also, we must keep in mind that the mutation rates are listed as number of mutations per individual per generation. This means that a mutation rate of 150 mutations per individual per generation adds up to 15 million mutations in a population of 100,000 individuals. If just 0.0001% of all those mutations becomes fixed this results in 150 mutations being fixed every generation. I would like to hear from MK why a 0.0001% fixation rate is impossible.

Lucky for me, someone has done the work on humant mutation rates. Even better, they were able to directly measure the human mutation rate by studying the de novo production of known Mendelian diseases through mutation. From this work they were able to establish a directly observed human mutation rate. Previously, other scientists had calculated the mutation rate needed in order to produce the observed divergence in human and chimp psuedogenes. The required mutation rate is 2.5 x 10(-8) per nucleotide per individual (diploid) per generation. The directly observed mutation rate is 1.8 x 10(-8). Given that both are based on a sliding scale of assumptions (average population density, average generation time, etc.) these two numbers agree quite well. You can find the paper here.

So my question to MK is this. What should the difference be according to your references and your calculations?

ERV's

This is the part where MK really lost me. I repeatedly stated that ERV's at the same genomic position found in multiple species should fit into a nested hierarchy. That is the evidence for common ancestry. So what does MK fire back with? PtERV's which are NOT FOUND AT THE SAME GENOMIC POSITION BETWEEN SPECIES!!!! I used the phrases "same genomic position" and "nested hierarchy" so many times that I can only assume that MK is intentionally ignoring the very basics of my argument.

Nowhere has MK tried to explain why there is a nested hierarchy between ERV's found at the same genomic position if all primates do not share a common ancestor, chimps and humans included. Nowhere. Do I need to mention "nested hierarchy" and "same genomic position" 150 times in a single paragraph before it is noticed?

 

[mark kennedy]

The link to Loudmouth's (LM's) phrase 'Nested Hierarchies' took me back to where it all started, Darwin's tree of life:

This is not a conclusion, it is an a priori assumption. Nested hierarchies simply sort according similarities and differences. The mechanism for the adaptive evolution that has come to be called positive/adaptive selection was the preservation of favored races according to Charles Darwin.

Although much remains obscure, and will long remain obscure, I can entertain no doubt, after the most deliberate study and dispassionate judgement of which I am capable, that the view which most naturalists entertain, and which I formerly entertained — namely, that each species has been independently created — is erroneous. I am fully convinced that species are not immutable; but that those belonging to what are called the same genera are lineal descendants of some other and generally extinct species, in the same manner as the acknowledged varieties of any one species are the descendants of that species. Furthermore, I am convinced that Natural Selection has been the main but not exclusive means of modification. (Introduction to On the Origin of Species by Charles Darwin)​

To this day evolutionists realize that the only alternative to the Darwinian Tree of Life is special creation.

Creation and evolution, between them, exhaust the possible explanations for the origin of living things. Organisms either appeared on the earth fully developed or they did not. If they did not, they must have developed from preexisting species by some process of modification. If they did appear in a fully developed state, they must indeed have been created by some omnipotent intelligence, for no natural process could possibly form inanimate molecules into an elephant or redwood tree in one step (Science On Trial: The Case For Evolution, by Dr. Douglas J. Futuyma)​

Talk Origins was not the first to propose grounds for the falsification of the Darwinian Tree of Life (not evolution or science but the naturalistic assumption of universal common ancestry). Charles Darwin himself made this bold and intellectually suicidal proposal:

We must suppose each new state of the instrument to be multiplied by the million; and each to be preserved till a better be produced, and then the old ones to be destroyed. In living bodies, variation will cause the slight alterations, generation will multiply them almost infinitely, and natural selection will pick out with unerring skill each improvement. Let this process go on for millions on millions of years; and during each year on millions of individuals of many kinds; and may we not believe that a living optical instrument might thus be formed as superior to one of glass, as the works of the Creator are to those of man?

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But I can find out no such case. No doubt many organs exist of which we do not know the transitional grades, more especially if we look to much-isolated species, round which, according to my theory, there has been much extinction. Or again, if we look to an organ common to all the members of a large class, for in this latter case the organ must have been first formed at an extremely remote period, since which all the many members of the class have been developed; and in order to discover the early transitional grades through which the organ has passed, we should have to look to very ancient ancestral forms, long since become extinct. (Darwin, Origin of SpeciesChapter 6 - Difficulties on Theory)​

I said all of that to show you this, we now know what would have had to be positively selected. It would have had to be the protein coding and regulatory genes, particularly those involved in the exponential growth of the human brain from that of apes. Before Homo Erectus burst on the scene less then 2 million years ago our ancestors would have been little more then apes:

Another debate centered around Homo habilis and Homo rudolfensis is whether or not these two species belong in the genus Homo or would be better suited in one of the other hominid genera. Some researchers feel that all species within the genus Homo should have characteristics, such as locomotor patterns, diet and body proportions, that make them more like modern humans than like the australopiths. These researchers feel that the characteristics of H. habilis and H. rudolfensis are more ape-like than modern, a conclusion that would remove them from our genus. The Homo habilis Debate​

From Homo habilis and Homo rudolfensis the cranial capacity would have had to double over night. What strikes me as dubious about all of this is that there are no fossils for the Chimpanzee ancestors from this period. In fact their ancestors are not represented from 5mya until very close to modern times. Hominids are represented by literally thousands of fossils, probably because every ape fossil is in natural history museums marked Homo XXX.

For thirty years everyone was told that there isn't enough of a difference in the protein coding genes to account for differences between apes and humans. What they told us was that the differences had to be the result of gene expression (see Evolution at Two Levels: On Genes and Form), this is what we now know about how the genes are expressed differently:

Overall, a total of 2014 genes or ~10% of genes analyzed differed in expression between humans and chimpanzees in at least one region of the brain (Supplemental Table 3). In general agreement, a total of 1234 genes were classified as being differentially expressed between humans and chimpanzees using more stringent criteria (p ≥ 0.95 or p ≤ 0.95 and ≥1.4-fold change).Regional Patterns of Gene Expression in Human and Chimpanzee Brains​

Ten percent are expressed differently but how many of the protein coding genes are different on an amino acid sequence level? Try 83% with 20% showing gross structural differences in their protein products. (Initial Sequence of Chimpanzee Chromosome 22, Nature).

In the opening lines of the Initial Sequence of the Chimpanzee Genome they credit Darwin's so called predictions with being spectacularly confirmed. Then in the discussion on the evolution of the protein coding genes they rejected natural selection as a major contributor.

More than a century ago Darwin and Huxley posited that humans share recent common ancestors with the African great apes. Modern molecular studies have spectacularly confirmed this prediction and have refined the relationships, showing that the common chimpanzee (Pan troglodytes) and bonobo (Pan paniscus or pygmy chimpanzee) are our closest living evolutionary relatives...

...here 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 humans. (Chimpanzee Genome, Nature 2005)​

That is just incredible, the mechanism that Darwin said was the main means wasn't a major contributor but his prediction is spectacularly confirmed? The nested hierarchies in Darwin's Tree of Life have been spectacularly falsified. The reason being that the differences cannot be accounted for by the known mutation rate. The burden of proof is on providing the directly observed and demonstrated mechanism for human evolution from that of apes. Evolutionists admit that they have no clue how and Darwin's natural selection was not a major contributor. So what was it then?

In a word, it would have had to be mutations, primarily indels (aka length mutations). It is well known that length mutations have the lowest mutation rate at 2.3 x 10^-9. They are 10 times less common then single substitutions and yet they account for almost three times more divergence. This is the table based on 1.33% divergence:

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Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.


Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
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Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000)​

When the actual divergence is found to be between 5% and 6% does the calculation of the mutation rate change? I'll tell you what, I'll get back to that one.

The ERVs are the final straw for me, this cryptic argument from Talk Origins are based on a paper that first proposed they be used as phenotype markers. At the time (2000) ERVs were thought to make up 1% of the human genome, now estimates are more like 8%. They have found the ERV class I (PtERV1 and PtERV2) have hundreds of insertion points with over a million base pairs involved that are specific to the chimpanzee genome. They are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon.

There are two major problems with this, first of all do you expect me to believe that 8% of the human genome is the result of germline mutations? That would mean that they have accumulated over 25 million years and at the same time the human lineage has adapted an immune system that has them teetering on the brink of extinction.

I point out that they have no clue what the molecular mechanism is that is responsible for the exponential growth of the human brain. The response is that it does not matter. I say it does matter for one key reason, science is about demonstrating hypothesis and at a crucial point in the series, demonstrating they can be formed into a valid theory. Sir Issac Newton proposed to the Royal Society in London that light was actually composed of seven colors and upon completion of the experimentum crucis demonstrated that it was indeed a valid theory. Had he went in there and said I am going to assume it's true no matter what the evidence is and despite the fact that I cannot prove it they would have laughed him out of the room.

It matters very much that they cannot demonstrate or directly observe the molecular mechanisms responsible for the most important evolutionary adaptation in our lineage. When they fail the burden of proof in this regard they have failed to provide a valid theory. Evolution itself is not in jeopardy, it is the false assumption of the common ancestor for humans and chimpanzees that is supported by an a priori assumption. Darwin's Tree of Life was based on the gradual accumulation of beneficial traits but the expansion of the human brain would require and overhaul of the most highly conserved genes known to modern genetics. Saying you don't know how it's possible is tantamount to admitting the common ancestor of chimps and humans is based on supposition and speculation.

Back in 2000 they thought the mutation rate was kind of high at 1.33%:

The average mutation rate was estimated to be 2.5 x 10-8 mutations per nucleotide site or 175 mutations per diploid genome per generation...Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. (Estimate of the Mutation Rate per Nucleotide in Humans, Genetics 200)​

How is it not a problem now that it is 5% to 6%?

What is more Transposable Elements are actually active and they are slowly finding out what they do:

These nonprotein-coding RNAs are encoded in gene introns and are involved in chemical modifications of selected bases of ribosomal RNAs. The article shows that new snoRNA copies were generated in vertebrate genomes via the copy-and-paste mechanism. Many of them are species-specific, and their insertion point was precisely determined by alignment with the corresponding genomic portion from a neighbour species. The mobilization of snoRNA gene sequences might ensure the presence of a functional copy when the parental one becomes invalidated by mutations. Moreover, such copies could evolve on their own to acquire the capacity of guiding new modifications of ribosomal RNAs.

Mammalian Small Nucleolar RNAs Are Mobile Genetic Elements

In my next post I am going to show why LM's source material is irrelevant as evidence of common ancestry. It should be obvious but so should the importance of demonstrating adaptive evolutionary mechanisms.

One last thing, we now know what the effects of mutations are on the human brain and neural functions and none of them are beneficial. With natural selection being dismissed as a major contributer we are left with supposition and speculation instead of proof. The ERVs like all the flawed homology arguments that proceeded it will eventually fall apart. The creationist doesn't even have to do all that much to help it along, scientists seem to be doing that all by themselves.

 

[Loudmouth]

MK’s most recent post is a magnificent example of “sleight of hand”. These magic tricks include the following:

1. Replacing the nested hierarchy with natural selection.
2. Replacing phenotypic variation with genetic variation.
3. Replacing the substitution rate with the indel rate in reference to the overall mutation rate.
4. Replacing “we don’t know right now” with “it’s impossible” in reference to brain evolution.
5. Replacing orthologous ERV’s with non-orthologous ERV’s.

MK has attempted to divert the reader’s attention from my main arguments. Hopefully this post will help the reader see through this smoke screen and help the reader understand why MK has fallen short of challenging my argument.

The Nested Hierarchy

MK attacks this concept by attacking the mechanism of directed change. The problem is that a nested hierarchy can be created in the absence of selection. One has nothing to do with the other. The nested hierarchy is created by the mechanisms of inheritance and speciation. In my first post I used the Romance Languages as an analogy, and it applies here as well. The divergence of the Romance Languages had nothing to do with Darwinian evolution or natural selection, and the nested hierarchy that these languages fall into have nothing to do with natural selection. No one is foolish enough to state that the Romance Languages can not be related because they are different. Quite the opposite. The Romance Languages are claimed to have a common ancestor because of their SIMILARITIES. The insistence that differences between species falsifies common descent and the nested hierarchy only serves to illustrates MK’s ignorance of what a nested hierarchy is.

MK was right in saying that a nested hierarchy is “simply sort[ed] according [to] similarities and differences.” He should have stopped there because that is as far as it goes. The nested hierarchy of life is the result of genetic isolation. For us and chimps, there is no mechanism that allows human DNA sequence to find it’s way into chimp populations (other than humans using genetic modification like that done in crops). Therefore, mutations or changes stay within a lineage. At the same time, genetic sequences found in the common ancestor of two populations is inherited by each lineage. This is why bats do not have feathers and why birds do not lactate. These phenotypes arose in each lineage after the mammal and avian lineages split.

While natural selection is proposed as a mechanism for promoting some phenotypes over others, it is by no means necessary to produce a nested hierarchy as is exemplified by the Romance Languages. A nested hierarchy is produced by a process of isolation, divergence, and accumulation of changes.

Phenotype vs. Genetic variability

MK also misrepresents a very basic concept that many people overlook: Evolution is blind to DNA sequence. That is, the process of evolution through natural selection does not select for changes in DNA. The process of evolution through natural selection does select for physical changes. This is a very important difference. MK quoted a paper which stated that “natural selection is not the major contributor to the large-scale patterns of genetic variability in humans.” Now, read the first two sentences of this paragraph and apply it to this statement. It is obvious where the disconnect has occurred. This would indicate that the majority of genetic variation between humans and chimps, and within each species, does not entail a phenotypic change (i.e. a physical change). This is consistent with the concept long held by geneticists that a vast majority of mutations are neutral with respect to phenotype or fitness. This would mean that the majority of physical differences (such as brain size) between humans and chimps is caused by a minority of the mutations that accumulated in the human lineage.

Mutation Rate

The next staple of MK’s oft repeated criticism of evolution is that the genetic differences are too high to be accounted for by the mutation rate. Again, MK gets it wrong. He compares apples to oranges, or more specifically the substitution rate to the indel rate. MK states that “Back in 2000 they thought the mutation rate was kind of high at 1.33% . . . How is it not a problem now that it is 5% to 6%.” MK didn’t seem to read either of his sources ver well. Guess what the 2000 estimate was based on? (drum roll please) Comparisons of human and chimp psuedogenes, a whole whopping 22 of them. So it would seem at the outset that MK is willing to accept the divergence calculated from 22 pseudogenes but not willing to accept the divergence calculated by the comparison of the entire genomes. Why is that?

Even worse, MK gets his terms mixed up. Guess what the chimp genome gives as the per nucleotide divergence? (drum roll please) 1.23%!!! To quote the actual paper, “We calculate the genome-wide nucleotide divergence between human and chimpanzee to be 1.23%, confirming recent results from more limited studies.” EGADS!! HOW CAN THIS BE? One simple reason. An indel is considered to be a single mutation. The 5-6% difference is the total DNA difference, but not the per nucleotide genome wide divergence.

Brain Evolution

This is the section where MK tries to turn “we don’t know” into “Goddidit”. Not knowing the genetic basis for the increase in human brain size is a “we don’t know right now”. However, work is being done on the question.

One hypothesis is that glial cell adhesion is a factor:
http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Another, fatty acid metabolism and fat metabolism play a pivotal role:
http://www.ncbi.nlm.nih.gov/sites/e...med.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

And yet another, that a mutation in an important muscle protein reduced the size of the lower jaw allowing for a larger cranium:
http://www.nature.com/nature/journal/v428/n6981/abs/nature02358.html

There are numerous hypotheses in addition to these which are being investigated by research groups across the world. So how is this a problem for evolution? MK still hasn’t told us.

Also, MK mentions that brain size had to double “overnight” at some point. I will point MK to the chart below. He will notice that the variation in cranium size for each species overlaps the species before and after it. Where did this doubling occur?

ERV’s

Guessing by MK’s reference of PtERV’s once again, he has never clued in on why ERV placement in the genome is such a big deal. I guess I will have to say those two phrases once again, and please listen this time MK: “NESTED HIERARCHY” “THE SAME SPOT IN THE GENOME”. Did you hear me this time MK? Do I really need to repeat this again in another post?

The reference I will be using is: Lineage-specific expansions of retroviral insertions within the genomes of African great apes but not humans and orangutans. Yohn et al., PLoS Biol. 2005 Apr;3(4):e110. Epub 2005 Mar 1.

And the linky: http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15737067

I included the title in hopes that it will clue MK in on the distribution of the ERV’s. As the paper states, these insertions are lineage specific. That is, the insertions occur after the lineages split from their common ancestor. How is this known? Again, those two little phrases that MK avoids like the plague: nested hierarchy and genomic placement.

In previous posts on ERV’s I have stated over and over that thousands of ERV’s are found at the same genomic position in both humans and chimps. When this is expanded to all primates, we again find thousands of ERV’s found at the same genomic position and those commonalities fall into a nested hierarchy which is expected if all primates share a common ancestor. So are PtERV1 and PtERV2 insertions shared at the same genomic position? Not the ones looked at thus far, just as would be expected if these ERV’s were inserted after a split from the common ancestor.

Let’s look at the specifics in the paper.

“Based on an analysis of 1,467 large-insert clones, we mapped 299 retroviral insertion sites among the four species. A total of 275 of the insertion sites mapped unambiguously to non-orthologous locations, indicating that the vast majority of elements were lineage-specific (i.e., they emerged after the divergence of gorilla/chimpanzee and macaque/baboon from their common ancestor).”

So now we are down to 24 insertions that did not “unambiguously map to non-orthologous locations”. In the paper’s parlance, orthologous=same genomic placement (down to the exact base). This means that “this would correspond to a maximum of 12 orthologous loci” This means that 275 out of 299 definitely map to different regions. This is in stark contrast to only ~300 ERV’s out of 200,000 that do not map to the same position between chimps and humans. Already we see that this is a poor comparison.

Due to the limitations of their methods, the authors of the paper were only able to narrow down these ERV’s to a general genomic position, not at the resolution needed to determine whether or not these ERV’s occur at orthologous positions. However, the macaque genome was recently sequenced as well as the chimp genome. This made it possible to determine whether or not 4 of these possible 12 (24 shared equals 12 loci) occur at orthologous positions. The authors concluded the following:

In one case, we were unable to refine the map interval owing to the presence of repetitive rich sequences within the interval. In two cases, we were able to refine the map location to single basepair resolution. Based on this analysis, we determined that the sites were not orthologous between chimpanzee and macaque. It is interesting to note that this level of refined mapping in chimpanzee revealed 4- to 5-bp AT-rich target site duplications in both cases. These findings are consistent with an exogenous retrovirus source since proviral integrations typically target AT-rich DNA ranging from 4 to 6 bp in length. Although the status of the remaining overlapping sites is unknown, these data resolve four additional sites as independent insertion events and suggest that the remainder may similarly be non-orthologous.​

So it is the conclusion of the authors that even those ERV’s that fall into the same genomic area are probably not at orthologous positions, and this is the definite case for 3 of them.

Unknowingly, MK has only strengthened my argument. If the same retroviral sequence is found in primates in a pattern that does not fit a nested hierarchy then these retroviral sequences should be found in non-orthologous positions. PtERV1 and 2 sequences are found in primates in a non-nested hierarchy. As the paper shows, and as the theory of evolution predicts, they are found at non-orthologous positions in the genome.

As to the overall content of retroviral associate sequence in the human genome, MK only has to look at the human genome paper. While ERV’s make up around 1%, retroviral related sequences (e.g. solo LTR’s, MaLTR’s) do make up 8% of the human genome. If MK wants to argue these numbers then I suggest he take it up with the author of the human genome paper.

And I am also scratching my head as to why it is a problem if the human genome is not currently under attack by retroviruses. Why is it a problem? We all know from recent history that retroviruses come and go, such as the modern emergence of HIV. Not only that, but a herpes-6 ERV was recently discovered in humans (source) proving that modern retroviruses are capable of integrating into the host germline resulting in an inheritable ERV. Even more, many ERV’s are heterologous in the human population. That is, there are people with an ERV not found in other humans in addition to the aforementioned herpes-6 insertion.

MK also states that transposable elements have function. Well, guess what? Function has nothing to do with my argument. It is the pattern of orthologous sequences that evidences common ancestry. The function or non-function of transposable elements, which aren’t even ERV’s, has nothing to do with my argument and I am curious how it contradicts the theory of evolution.

Conclusion:

MK has tried to misrepresent my argument both by sleight of hand and through inconsequential evidence. My argument still stands as written. The pattern of orthologous ERV’s evidences common ancestry. Citing non-orthologous ERV’s does nothing to diminish this argument. Whether or not we understand the genetic basis of human brain evolution does not cast doubt on the theory of evolution, nor does the genetic distance between humans and chimps. MK can keep repeating these claims, but they ring hollow for one reason: incredulity is not evidence.

 

[mark kennedy]

MK’s most recent post is a magnificent example of “sleight of hand”. These magic tricks include the following:

1. Replacing the nested hierarchy with natural selection.

LM linked his term 'nested hierarchy' to this Talk Origins discussion on Darwin's Tree of Life. Charles Darwin on Classification and the Nested Hierarchy. The full title of Darwin's famous On the Origin of Species was 'On the Origin of Species: by Means of Natural Selection, or the Preservation of Favored Races in the Struggle for Life'. I simply followed the link and went from there and none of the carefully prepared discussion on Darwin's book or the Chimpanzee Genome paper was addressed. Darwin offered a basis for falsification of the proposed mechanism but LM chose to ignore this and go straight to the Ad hominem when it was his link that led to the discussion of natural selection in the first place. What is even more telling is that not one point raised was even addressed.

2. Replacing phenotypic variation with genetic variation.

Genetics is focused on how alleles are expressed in the phenotype from the gene. In fact one of the most common ways for geneticists to know what genes do is to knock one out. The only way we could have evolved from apes is accelerated restructuring of highly conserved genes. Not just the 4% of the protein coding genes that would have had to have accelerated evolutionary rates. At least one highly conserved regulatory gene would have had to have 18 substitutions in a gene that has not changed significantly since the Cambrian Explosion:

"The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain. We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal– Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology."

The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400Myr ago​

​

See FIGURE 2 from An RNA gene expressed during cortical development evolved rapidly in humans. (Nature 443, 167-172 14 September 2006)

3. Replacing the substitution rate with the indel rate in reference to the overall mutation rate.

Notice the central question is not answered, if the divergence jumps from 1.33% to 5% does the mutation rate change? I simply pointed out the the indel rate was an order of magnitude lower then single base substitutions. There has been no reply.

4. Replacing “we don’t know right now” with “it’s impossible” in reference to brain evolution.

When it comes to the expansion of the human brain is size and complexity modern genetics doesn't have a clue. One thing has become crystal clear, the level of divergence far exceeds what they have been telling us the the last half a century.

5. Replacing orthologous ERV’s with non-orthologous ERV’s.

That is the one I have been waiting for, here is the initial statement LM made without a shred of supporting evidence:

Luckily for us, both the human and chimp genomes have been sequenced. The results? Out of the ~200,000 ERV’s present in the human genome only 82 are not found in the chimp genome. In the chimp genome, only 280 can not be found in the human genome.

There is nothing in the Chimpanzee Genome paper supporting this obviously erroneous statement. Every evolutionist on the net brings up the ERV orthologues. For one thing there are 234 Class I ERVs in the Table 2 of the Chimpanzee Genome paper that have no othologues in the human genome. Now it is true that of the 42 families of full length ERVs that have been unambiguously only two do not have some othologues. Class I ERV family PTERV1 has 100 members and is one of the most abundant families of ERVs in the Chimpanzee genome. I don't know where LM is getting his facts but it's not from the Chimpanzee Genome paper and it's not from here:

"We report here that the chimpanzee genome contains at least 42 separate families of endogenous retroviruses, nine of which were not previously identified. All but two (CERV 1/PTERV1 and CERV 2) of the 42 families of chimpanzee endogenous retroviruses were found to have orthologs in humans. Molecular analysis (PCR and Southern hybridization) of CERV 2 elements demonstrates that this family is present in chimpanzee, bonobo, gorilla and old-world monkeys but absent in human, orangutan and new-world monkeys. A survey of endogenous retroviral positional variation between chimpanzees and humans determined that approximately 7% of all chimpanzee-human INDEL variation is associated with endogenous retroviral sequences."

Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses
Genome Biol. 2006

That is not the only blatant error, every time LM makes a point it's based on erroneous facts, for instance:

As to the overall content of retroviral associate sequence in the human genome, MK only has to look at the human genome paper. While ERV’s make up around 1%, retroviral related sequences (e.g. solo LTR’s, MaLTR’s) do make up 8% of the human genome. If MK wants to argue these numbers then I suggest he take it up with the author of the human genome paper.

This is just plain wrong:

Fig. 1. Classification of transposable elements. The percentage of each element in the genome and the estimated number of the elements of the main groups are indicated.

Retroelements and the human genome: New perspectives on an old relation

This time I know where he is getting his information, he is taking it from an outdated argument on Talk Origins. The current evidence is not indicating a smoking gun by any stretch. In fact, the ERVs are actually another problem for a common ancestor. In fact CERV 2 (Chimpanzee ERV) has an estimated age of 21.9 mya to 14.1 mya with no human orthologues. The CERV1/PtERV1 with 100 members is estimated between 5 mya and 7.8 mya. That means that the most abundant ERVs in the Chimpanzee Genome came about before or right around the split That means in addition to the adaptive evolution of the human brain our ancestors would have had to adapt their immune system to push these ERVs to the brink of extinction.

Also, MK mentions that brain size had to double “overnight” at some point. I will point MK to the chart below. He will notice that the variation in cranium size for each species overlaps the species before and after it. Where did this doubling occur?

A. Afarensis with a cranial capacity of ~430cc lived about 3.5 mya.
A. Africanus with a cranial capacity of ~480cc lived 3.3-2.5 mya.
P. aethiopicus with a cranial capacity of 410cc lived about 2.5 mya.
P. boisei with a cranial capacity of 490-530cc lived between 2.3-1.2 mya.
OH 5 'Zinj" with a cranial capacity of 530cc lived 1.8 mya.
KNM ER 406 with a cranial capacity of 510cc lived 1.7 million years ago.

Where does it double?

"The skeleton was about 1.60 m (5 ft 3 in) tall, although he might have been 68 kg (150 lb) and 1.85 m (6 ft 1 in) tall had he lived to adulthood. The total skeleton is made up of 108 bones accounted for. The cranial capacity of Turkana Boy was about 880 cc, although if he had lived to adulthood, it would have been about 910 cc"

Turkana Boy, Wikipedia

Hexian 412,000 years old had a cranial capacity of 1,025cc.
ZKD III (Skull E I) 423,000 years old had a cranial capacity of 915cc.
ZKD II (Skull D I) 585,000 years old had a cranial capacity of 1,020cc
ZKD X (Skull L I) 423,000 years ago had a cranial capacity of 1,225cc
ZKD XI (Skull L II) 423,000 years ago had a cranial capacity of 1,015cc
ZKD XII (Skull L III) 423,000 years ago had a cranial capacity of 1,030cc
Sm 3 >100,000 years ago had a cranial 917cc
KNM-WT 15000 (Turkana Boy) 1.5 million years ago had a cranial capacity of 880cc
(Source: Endocranial Cast of Hexian Homo erectus from South China, AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 130:445–454. 2006)

That is where it doubled LM, at adulthood Turkana Boy would have had a cranial capacity of 910cc or close to twice that of the African apes who are considered our ancestors. Then the cranial capacity remained static until 100,000 years ago. Let us not forget that by some other equally mysteries evolutionary process the Neanderthals developed a cranial capacity 10% greater then our own.

That is in addition to the fact that we have no chimpanzee ancestors to compare the cranial capacity to. That is because every ape skull unearthed in Africa and Asia is automatically celebrated as one of our ancestors in a desperate attempt to find this mythical transitional apeman.

One thing is clear, these Talk Origins arguments are grossly outdated and yet retain their popularity.

Conclusion:

MK has tried to misrepresent my argument both by sleight of hand and through inconsequential evidence. My argument still stands as written. The pattern of orthologous ERV’s evidences common ancestry. Citing non-orthologous ERV’s does nothing to diminish this argument. Whether or not we understand the genetic basis of human brain evolution does not cast doubt on the theory of evolution, nor does the genetic distance between humans and chimps. MK can keep repeating these claims, but they ring hollow for one reason: incredulity is not evidence.

I'm not the one making an argument from ignorance. I say again, the theory of evolution is not in jeopardy here, the flawed Darwinian a priori assumption of a common ancestor for humans and chimpanzees is. There is nothing credible to argue against, just the same tired Talk Origins propaganda rehashed in circles.

I saved the best for last:

The next staple of MK’s oft repeated criticism of evolution is that the genetic differences are too high to be accounted for by the mutation rate. Again, MK gets it wrong. He compares apples to oranges, or more specifically the substitution rate to the indel rate. MK states that “Back in 2000 they thought the mutation rate was kind of high at 1.33% . . . How is it not a problem now that it is 5% to 6%.” MK didn’t seem to read either of his sources ver well. Guess what the 2000 estimate was based on? (drum roll please) Comparisons of human and chimp psuedogenes, a whole whopping 22 of them. So it would seem at the outset that MK is willing to accept the divergence calculated from 22 pseudogenes but not willing to accept the divergence calculated by the comparison of the entire genomes. Why is that?

Even worse, MK gets his terms mixed up. Guess what the chimp genome gives as the per nucleotide divergence? (drum roll please) 1.23%!!! To quote the actual paper, “We calculate the genome-wide nucleotide divergence between human and chimpanzee to be 1.23%, confirming recent results from more limited studies.” EGADS!! HOW CAN THIS BE? One simple reason. An indel is considered to be a single mutation. The 5-6% difference is the total DNA difference, but not the per nucleotide genome wide divergence.

The chart on mutation rates I quoted, cited and linked was based on 1.33% divergence. The Chimpanzee Genome paper found 1.23% divergence with 1.06% being fixed. However, they measured the DNA difference in base pairs.

"The analysis of modest-sized insertions reveals ~32 Mb of human-specific sequence and ~35 Mb of chimpanzee-specific sequence, contained in ~5 million events in each species...

...approx70,000 indels larger than 80 bp comprising 73% of the affected base pairs)...

...larger insertions (> 15 kb) identified 163 human regions containing 8.3 Mb of human-specific sequence...

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions"​

That's 5 million mutation events that measure 90 million base pairs. This is the most fundamental error yet, DNA is measured in base pairs.

​

When the double helix is unzipped the single strand is an unpaired nucleotide sequence.

​

Of course they measure mutations by nucleotides whether paired up in DNA strands or single nucleotide sequences like the RNA. It is the height of ignorance to declare that they do not.

 

[Loudmouth]

Again, I will be breaking down this response into multiple categories to keep everything straight.



1. Nested Hierarchy

Linnaeus was the first to recognize that life fell into a nested hierarchy in the 1700’s, one hundred years before Darwin wrote Origin of Species. The nested hierarchy has never depended on the theory of evolution. The nested hierarchy is an observation which the theory of evolution attempts to explain through a specific mechanism: descent with modification. Even without natural selection, descent with modification in combination with speciation produces a nested hierarchy. So we have two facts that converge on the same answer. First, the fact that life falls into a nested hierarchy. Second, the fact that the mechanisms of speciation and descent with modification produce a nested hierarchy. If MK wants to argue otherwise please do. I know of no other pattern that evolution is capable of producing other than a nested hierarchy. I know of no other pattern that both extant and extinct species fall into.

Claiming that such and such subset of sequence was not affected by natural selection does nothing to get rid of the fact that life falls into a nested hierarchy, both at the morphological and genetic level. MK quotes a paper which accurately states that the majority of divergent sequence and species specific variation is not due to natural selection. I see no reason to disagree. However, this means that a minority of sequence has been influenced by natural selection. I will repeat, there is human DNA sequence that has been influenced by natural selection. MK acts as if none of the DNA has gone through natural selection, but his own references argue otherwise. Both the chimp genome paper and the HAR1 paper state unequivocally that human DNA sequences have undergone natural selection. So much for natural selection not existing, much less nested hierarchies.



2. Phenotype and Genotype, Brain size

MK argues that no one knows the genetic basis for the increase in brain size in the human lineage. He then goes on to state that it requires overhauling a specific set of genes. So which is it MK? Is it known or unknown? Are mutations in HAR1 responsible for the increase in human brain size, or not? What fraction of DNA changes between humans and chimps is directly responsible for increased brain size? What fraction of DNA changes between humans and chimps is responsible for all divergent phenotypes? Is DNA divergence between humans and chimps responsible or not responsible for the larger brain size in humans? Until this is answered MK can not state what is impossible, improbable, or problematic. What remains is that the morphology and genetics of all apes falls into a nested hierarchy as predicted by the theory of evolution and common descent. In my book, facts that fulfill the predictions of a theory count as evidence in support of a theory.

I really want MK to flesh out this argument. It looks to me to be nothing other than a God of the Gaps argument. Scientists don’t know the specific genetic changes that were necessary for a large human brain, therefore Goddidit. How does this make sense? Does any scientist doubt that the genetic basis is found in the divergent sequence between humans and chimps? Not at all. In fact, MK’s very own material highlights that common ancestry is being used to search for the genetic basis, specifically:

The developmental and evolutionary mechanisms behind the emergence of human-specific brain features remain largely unknown. However, the recent ability to compare our genome to that of our closest relative, the chimpanzee, provides new avenues to link genetic and phenotypic changes in the evolution of the human brain.​

Now why would the chimp genome sequence give new avenues for research? How does that work MK? Could it be that common ancestry is being APPLIED as a research tool. Me thinks so.

As far as fossil species, the graph I listed clearly shows that the variation in brain size between each transitional species overlaps both the species before it and the species after it. How can this be considered a “doubling in brain size overnight” when each group overlaps the other?

Here is another graph. It graphs a more important comparison, brain size of all individuals. As you will see the cranium size between each species overlaps, refuting the claim that a doubling happened overnight between each species. MK is using nothing more than a smoke screen. He uses the extremes at either end of each species variation to make the reader think there was a doubling. This is dishonest in the extreme. MK acts as if there is only one representative fossil for each species. There isn’t.

source.


3. Genetic divergence

MK’s push as far as DNA divergence is that a 5% divergence produces a very high deleterious mutation rate. He claims that between then and there that the divergence went from 1.33% to 5-6%. It didn’t. Between earlier papers and the chimp genome paper the divergence went down, from 1.33% to 1.23% (pg. 71 of the chimp genome paper). Remember, MK is arguing from a rate of divergence that produces a deleterious mutation rate that is too high. I would like to know why MK is misleading the public on this one.

The problem is that MK is comparing apples and oranges. To calculate the deleterious mutation rate you compare the genomes mutation event to mutation event. What the deleterious mutation rate looks for is the chance of a mutation (substitution or indel) destroying an important reading frame or gene. That is the deleterious mutation rate. Therefore, the 1.23% nucleotide divergence rate is the correct number to use, not the overall DNA base difference which turns a single 7,000 bp indel mutation into 7,000 changes. An indel is a single mutation, even if it involves several base pairs.

No one has been lying to the public or trying to cover things up. Each figure, be it 1.23% or 5-6%, carries very specific qualifiers and importance when looking at population genetics. MK has yet to understand this difference. He is howling at a wind he does not understand.

4. ERV’s

Orthologous ERV’s fall into a nested hierarchy with very, very, very few exceptions. PtERV’s are not one of those examples. PtERV’s are not found at orthologous locations in different species. This is expected if PtERV’s inserted into these lineages independently in each lineage after each lineage diverged from the common ancestor of all apes (including humans). This is the argument I have made time and time again. MK has decided to disregard the orthologous nature of ERV’s and instead focus on their distribution (orthologous or not). Why is this? What is MK trying to prove other than he does not understand my argument? If MK only answers one question in this section I hope it will be this one: Of all the PtERV’s and CERV’s found in different primate species, how many of them are unambiguously found at the same base in the genome (ie orthologous positions)?

Let’s take a step back for a moment and do the math. I am going to be really generous and state that each retrovirus has 100 insertion sites to choose from. In reality, this number should be in the thousands for each virus but a few select viruses can be selective at times, so 100 is a worst case scenario. Now, what are the chances that chimps and humans will share 200,000 ERV’s at the same insertion site by chance? That probability is 1 in 200,000 to the 100th power, or 1 in 1.2 x 10^(530). That’s a 12 with 529 zeros after it. Therefore, the odds of humans and chimps NOT sharing common ancestry is 1 in 12 with 529 zeros after it. Looks like MK has bet on the underdog.

How do I know that there are nearly 200,000 ERV’s shared by chimps and humans. From the human and chimp genome papers that I linked to at the bottom of my first and opening post. In Table 11 of the human genome paper on pg. 880 it lists the following information. There are 112,000 ERV class I insertions, 8,000 ERV(K) class II insertions, and 83,000 ERV(L) class III insertions (note: the column heading has a multiplier [x1000]). That adds up to 203,000 insertions. I simply shortened it to 200,000 because it’s a nice round number. In Table 2 of the chimp genome paper on pg. 75 it lists lineage specific transposable elements which includes some ERV class I and II elements. Lineage specific ERV’s are those that are not found in the other genome at the same genomic position. Table 2 lists a total of 277 ERV’s found in chimps that are not found in humans. In the human genome, of the 200,000 ERV’s described in the human genome paper only 82 are not found in the chimp genome. This means that only 0.04% of the ERV’s found in humans are not found in chimps at the same exact genomic position, and conversely only 0.14% of ERV’s found in chimps are not found in humans. That’s a lot of shared retroviral insertions at the same base in the genome, I don’t care who you are.

I was incorrect, however, in relation to the percentage of the genome consisting of ERV’s. If we combine all three classes of ERV’s (from Table 11 from the human genome paper) they comprise approximately 4.64% of the human genome. I really don’t know how this falsifies common descent, but we will see what kind of stink MK makes of this.

Conclusion:

MK argues that brain size doubled overnight. It didn’t. MK argues that the divergence rate went from 1.33 to 5-6%. It didn’t, it actually went down to 1.23%. I incorrectly stated that ERV’s comprise 1% of the genome, but this is inconsequential to the argument. My argument is that the placement of the ERV’s in the genome and the distribution of orthologous ERV’s evidences evolution, and it does. MK thinks that non-orthologous ERV’s refute this claim when clearly they don’t. The chances of humans and chimps not sharing common ancestry (according to ERV's) is 1 in 12 with 529 zeros after it.

 

[mark kennedy]

​

FIGURE 2. Comparative neuroanatomy of humans and chimpanzees. (Genetics and the making of Homo sapiens. Nature April 2003)

MK argues that no one knows the genetic basis for the increase in brain size in the human lineage. He then goes on to state that it requires overhauling a specific set of genes.

The molecular mechanism is unknown, the differences in human specific brain related, highly conserved and functionally biased genes are characterized in the scientific literature that you do not bother to read.

Are mutations in HAR1 responsible for the increase in human brain size, or not? What fraction of DNA changes between humans and chimps is directly responsible for increased brain size? What fraction of DNA changes between humans and chimps is responsible for all divergent phenotypes? Is DNA divergence between humans and chimps responsible or not responsible for the larger brain size in humans?

An RNA regulatory gene without significant substitutions since the Cambrian suddenly gets 18. This is accelerated evolution and while extraordinary, it is not the only gene that would have required a massive overhaul. With no directly observed or demonstrated mechanism you have supposition and speculation to support common ancestry, not science.

Scientists don’t know the specific genetic changes that were necessary for a large human brain, therefore Goddidit. How does this make sense?

It doesn't and neither does Goddidnt do it.

Does any scientist doubt that the genetic basis is found in the divergent sequence between humans and chimps?

They search for the genetic basis but it alludes them. The a priori assumption that there is a common ancestor is never questioned.

As far as fossil species, the graph I listed clearly shows that the variation in brain size between each transitional species overlaps both the species before it and the species after it. How can this be considered a “doubling in brain size overnight” when each group overlaps the other?

The scattergram has no details, specifics or reliable reference material. A bunch of dot's on a page you get from Panda's Thumb is not an argument, it's not evidence, it's a dodge. You asked where the doubling occurred, I showed you with precise specifics and detailed information you simply ignore.

MK is using nothing more than a smoke screen. He uses the extremes at either end of each species variation to make the reader think there was a doubling. This is dishonest in the extreme. MK acts as if there is only one representative fossil for each species. There isn’t.

I use peer scientific literature with specific fossils and identify the time and cranial capacity. I'm not embedding a couple of scattergrams from a propaganda mill, I actually read the scientific literature. The cranial capacity jumped from about 500cc to 1000cc overnight and remained static for at least a million years. That is after it had remained static for at least three million years since the split. That plus the fact that the chimpanzee lineage disappears 5 mya should be telling you something but you habitually ignore the facts.

MK’s push as far as DNA divergence is that a 5% divergence produces a very high deleterious mutation rate. He claims that between then and there that the divergence went from 1.33% to 5-6%. It didn’t. Between earlier papers and the chimp genome paper the divergence went down, from 1.33% to 1.23% (pg. 71 of the chimp genome paper). Remember, MK is arguing from a rate of divergence that produces a deleterious mutation rate that is too high. I would like to know why MK is misleading the public on this one.

The single base substitution rate varies between 1% and 2% depending on which sequence is being compared. The indels were not discovered until fairly recently and that adds another 3% to 4% to the known divergence. The Chimpanzee Genome paper says so in no uncertain terms and I am not the one lying to the public. You have made another erroneous statement with the facts right in front of you. I will give you the benefit of a doubt and assume you are just arguing from ignorance rather then willful deception.

The problem is that MK is comparing apples and oranges. To calculate the deleterious mutation rate you compare the genomes mutation event to mutation event. What the deleterious mutation rate looks for is the chance of a mutation (substitution or indel) destroying an important reading frame or gene. That is the deleterious mutation rate. Therefore, the 1.23% nucleotide divergence rate is the correct number to use, not the overall DNA base difference which turns a single 7,000 bp indel mutation into 7,000 changes. An indel is a single mutation, even if it involves several base pairs.

There are 5 million indels that cumulatively represent 90 million base pairs of divergence. There are 35 million single base substitutions that represent 35 Mb of divergence. Taken together we are looking at 125 Mb (million base pairs). I have quoted cited and linked the most complete sequence and comparison of the DNA of humans and chimpanzees. You are making these ridiculas rationalizations that are contradicted by the facts.

No one has been lying to the public or trying to cover things up. Each figure, be it 1.23% or 5-6%, carries very specific qualifiers and importance when looking at population genetics. MK has yet to understand this difference. He is howling at a wind he does not understand.

The only qualifier is whether or not you count the indels:

"This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies"​

They cite the following papers as supporting evidence:

Fortna, A. et al. Lineage-specific gene duplication and loss in human and great ape evolution. PLoS Biol. 2, E207 (2004)

Britten, R. J. Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels. Proc. Natl Acad. Sci. USA 99, 13633–13635 (2002)

Frazer, K. A. et al. Genomic DNA insertions and deletions occur frequently between humans and nonhuman primates. Genome Res. 13, 341–346 (2003)

Locke, D. P. et al. Large-scale variation among human and great ape genomes determined by array comparative genomic hybridization. Genome Res. 13, 347–357 (2003)

Liu, G. et al. Analysis of primate genomic variation reveals a repeat-driven expansion of the human genome. Genome Res. 13, 358–368 (2003)​

Orthologous ERV’s fall into a nested hierarchy with very, very, very few exceptions.

This has already been proven false, the ERVs are categorized into 42 families, 40 of which have orthologues. The most abundant class of ERVs do not have orthologues which I have demonstrated repreatedly.

PtERV’s are not one of those examples. PtERV’s are not found at orthologous locations in different species. This is expected if PtERV’s inserted into these lineages independently in each lineage after each lineage diverged from the common ancestor of all apes (including humans). This is the argument I have made time and time again. MK has decided to disregard the orthologous nature of ERV’s and instead focus on their distribution (orthologous or not). Why is this? What is MK trying to prove other than he does not understand my argument? If MK only answers one question in this section I hope it will be this one: Of all the PtERV’s and CERV’s found in different primate species, how many of them are unambiguously found at the same base in the genome (ie orthologous positions)?

First of all there are only 11 substitutions identified that Talk Origins based it's bogus probability statistics on. Second of all you have offered nothing but bogus evidence supporting you claim that virtually all ERVs are identical in the two genomes. You said there are only 82 but that the other 200,000 or exactly the same. I proved you wrong.

Two CERV families have no human orthologues

CERV 1/PTERV1
With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. CERV 1/PTERV1 elements range in size from 5 to 8.8 kb in length, are bordered by inverted terminal repeats (TG and CA) and are characterized by 4 bp TSDs...Phylogenetic analysis of the LTRs from full-length elements of CERV 1/PTERV1 members indicated that this family of LTRs can be grouped into at least two subfamilies (bootstrap value of 99; Figure 3). The age of each subfamily was estimated by calculating the average of the pairwise distances between all sequences in a given subfamily. The estimated ages of the two subfamilies are 5 MY and 7.8 MY, respectively, suggesting that at least one subfamily was present in the lineage prior to the time chimpanzees and humans diverged from a common ancestor (about 6 MYA). This conclusion, however, is inconsistent with the fact that no CERV 1/PTERV1 orthologues were detected in the sequenced human genome.
Genome Biol. 2006​

Let’s take a step back for a moment and do the math. I am going to be really generous and state that each retrovirus has 100 insertion sites to choose from. In reality, this number should be in the thousands for each virus but a few select viruses can be selective at times, so 100 is a worst case scenario. Now, what are the chances that chimps and humans will share 200,000 ERV’s at the same insertion site by chance?

Potential insertion sites are irrelevant you have yet to support your statement that there are 200,000 of the same ERVs at the same insertion site. The Human Genome Project reported that there are nearly 200,000 ERV’s sure enough but never compared them to Chimpanzee ERVs.

ERV class I 112,000
ERV (K) class II 8,000
ERV (L) class III 83,000

For a total of 203,000 human genome ERVs taken from the initial sequence of the Human genome. There was approximately 443,000 LTR elements total. You still have not shown a comparison that makes all but 82 of them identical to the chimpanzee.

In Table 2 of the chimp genome paper on pg. 75 it lists lineage specific transposable elements which includes some ERV class I and II elements. Lineage specific ERV’s are those that are not found in the other genome at the same genomic position. Table 2 lists a total of 277 ERV’s found in chimps that are not found in humans. In the human genome, of the 200,000 ERV’s described in the human genome paper only 82 are not found in the chimp genome.

I know where you are getting the 200,000 ERVs now but where you are getting the 82 not found in the Chimpanzee genome is still a mystery.

I was incorrect, however, in relation to the percentage of the genome consisting of ERV’s. If we combine all three classes of ERV’s (from Table 11from the human genome paper) they comprise approximately 4.64% of the human genome. I really don’t know how this falsifies common descent, but we will see what kind of stink MK makes of this.

That was an early estimate, the latest and greatest you have already been shown repeatedly.

​

Conclusion: MK argues that brain size doubled overnight. It didn’t.

It doubled 2 million years ago from Homo habilis to Homo erectus as I demonstrated.

MK argues that the divergence rate went from 1.33 to 5-6%.

It's 5% counting indels but without counting chromosomal rearrangements which are another 20 million base pairs. "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." Proc Natl Acad Sci U S A. 2002

Estimates of nucleotide substitution rates of aligned sequences range from 1.23% by bacterial artificial chromosome (BAC) end sequencing to about 2% by molecular analysis, whereas the overall sequence difference was estimated to be approximately 5% by taking regions of insertions or deletions (indels) into account. DNA sequence and comparative analysis of chimpanzee chromosome 22, Nature 2004

MK argues that brain size doubled overnight. It didn’t. MK argues that the divergence rate went from 1.33 to 5-6%. It didn’t, it actually went down to 1.23%. I incorrectly stated that ERV’s comprise 1% of the genome, but this is inconsequential to the argument. My argument is that the placement of the ERV’s in the genome and the distribution of orthologous ERV’s evidences evolution, and it does. MK thinks that non-orthologous ERV’s refute this claim when clearly they don’t. The chances of humans and chimps not sharing common ancestry (according to ERV's) is 1 in 12 with 529 zeros after it.

The single base pair divergence went down, overall it went up to at least 5%. ERVs make up ~8% of the human genome by the latest estimates. The Human Genome Project did report some 200,000 ERVs in the Human genome but they did not compare them to Chimpanzee ERVs. LMs 12 with 528 zeros is a fabrication of the highest order and his posts are riddled with fundamental errors. The most blatantly obvious is his insistence that the divergence actually went down to 1.23%. There can only be two possible explanations for this:

One: LM does not know what a base pair is or how genomes are measured.
Two: LM does not want to count the indels.

If it's the first option then we are dealing with an argument from ignorance. If it's the second option then it's willful deception and if that is the case then it's not the first time I have encountered it.

Google 'Chimpanzee Genome' and at the top you will find this statement from Nature Magazine announcing the Genome paper:

What makes us human? We share more than 98% of our DNA and almost all of our genes with our closest living relative, the chimpanzee. The chimpanzee genome​

THE ACTUAL PAPER SAYS OTHERWISE. We share no more the 95% of the same DNA, only 29% of the genes are the same and they know it. Now you know it whether you believe it or not, whether you like it or not, whether you want to admit it or not.

 

[Loudmouth]

It's time to wrap this debate up. This post will serve as a conclusion to my side of the debate.

MK has challenged the concept of human/chimp common ancestry in several ways.

1. The measured DNA divergence would result in a detrimental mutation rate that is too high for any species to accomodate.

2. The genetic basis of human brain development is unknown. MK argues that this is due to the fact that scientists are using a failed paradigm, namely common descent.

3. There was a sudden increase in brain size between H. habilis and H. erectus. A quick note, MK is a "lumper" in fossil speak. Some taxonomists classify early H. erectus as H. ergaster.

There are other minor arguments, but I hope that MK agrees that this is the meat of his argument.

DNA divergence

In post #4 MK stated the following:

Back in 2000 they thought the mutation rate was kind of high at 1.33%:
The average mutation rate was estimated to be 2.5 x 10-8 mutations per nucleotide site or 175 mutations per diploid genome per generation...Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. (Estimate of the Mutation Rate per Nucleotide in Humans, Genetics 200)

How is it not a problem now that it is 5% to 6%?

The deleterious mutation rate is based on mutational events, not the size or mechanism of the mutation itself. The deleterious mutation rate is based on the concept that knocking out a gene is bad for the organism. Therefore, any mutation which prevents a gene from producing a functional protein is considered deleterious. In this case there is no difference between a single base substitution and the insertion of seven thousand base pairs. Both mutational events produce the same result. Therefore, the correct figure to use when calculating the deleterious mutation rate is the rate at which mutational events occur. In the first estimate (the one quoted above) they used around 20 psuedogenes shared by chimps and humans to calculate the rate at which mutation events occur. They treated indels and substitutions equally. The did not count a 5 base pair indel as five separate events but as one event. From this they calculated a divergence of 1.33%. When the entire chimp genome was sequenced this same analysis showed a 1.23% divergence.

The 5% to 6% that MK harps on is not the correct figure for calculating the deleterious mutation rate. That figure is the total divergence of all DNA bases, not the divergence due simply to mutation events. MK's argument is impotent at this point. MK is not using the correct rate for calculating the deleterious mutation rate. If MK wants to argue that the divergence is still too high I guess I can't stop him, but he can't use the deleterious mutation rate as a reason for rejecting common ancestry.

Genes and the Human Brain

MK's argument can be summed up thus:

From post #2
Researchers are unanimous in admitting that they have no clue how the most significant human trait was produced and yet insist that the case for a common ancestor has been made.

The argument for common descent is not based on the genetic basis for human brain size. It is based on shared characteristics in each genome. MK's argument falls flat right away. MK has also not shown a link between not being able to determine the genetic basis for human brain development and common descent. I am sure no geneticist could give me a genetic basis for the differences between me and my siblings, but this doesn't change the fact that me and my siblings share a common ancestor. It is quite obvious that not knowing the genetic basis for differences between two species has nothing to do with the evidence for common descent.

The closest he comes to any explanation is that he thinks there are too many mutations in the gene har1A. However, this is exactly what we would expect to see in a gene that is under strong selection. Nowhere has MK shown that the differences between the chimp and human har1A gene result in a deleterious phenotype. Nowhere has MK shown that individuals between humans and our proposed common ancestor with chimps suffered from mutations in har1A.

MK even goes as far as to state that brain related genes can not withstand mutations. This is laughably false. I would suggest that MK visit the homepage for the Human Haplotype Project (www.hapmap.org). If you do a search using the word "brain" it will give you hundreds of brain related genes. A quick perusal will demonstrate that there are widspread single nucleotide polymorphisms (SNP's) spread throughout the human population in these brain related genes. I even dug through databases and found the stretch of DNA that codes for har1A (aka har1F). Guess what? There are two common mutations in this RNA gene. Go figure. If anyone wants to go through the hassle of figuring out how to search for genes and find them at the haplotype project website PM me and I will walk you through it the best I can.

So where does this leave MK's argument? Nowhere, from where I am sitting. It's based on two logical fallacies, an argument from ignorance and an argument from incredulity. First, MK argues that because we don't currently know the genetic basis for brain development that God did it, or the equivalent evolution-didn't-do-it. Then MK uses his own incredulity in the number of mutations in the har1A gene to support the argument that this gene did not evolve. Nowhere has MK produced a positive evidence for his argument.

The Fossils

MK argues that brain size doubled between H. habilis and H. erectus. It is important to note that early H. erectus, sometimes classified as H. ergaster, had a slightly smaller brain capacity than late H. erectus. Also, an important factor in comparing brain size is the overall size of the specimen. Within species there is a direct correlation between brain size and overall body size. Therefore, the best comparison is brain size with respect to overall body size. When this comparison is done H. habilis specimens and early H. erectus specimens overlap. The variation within each species overlaps the other. There is no doubling overnight as MK claims. From McHenry, Henry, "Tempo and Mode in Human Evolution", 1994, PNAS vol. 91 pg. 6785:

With either taxonomy, the absolute brains sizes of these early Homo specimens lie between Australopithecus and H. erectus, although relative brain sizes of early members of H. erectus overlap the range of the smaller-bodied specimens of H. habilis​

So much for a doubling overnight. The graph from post #5 is also from this paper, and it also demonstrates that Homo species overlap in relative brain size. I would also suggest that MK read the entire paper as it does a good job of outlining the trends in human evolution as evidenced in the fossil record.

Unlike MK, the author of the paper uses several specimens from each species for the comparison. Cherry picking data is not the honest thing to do, and that is exactly what MK has done, either intentionally or unintentionally. If MK has a more recent peer reviewed paper on the comparison between H. habilis and H. erectus I am all ears (or eyes).

Now I am going to move to my own arguments supporting common ancestry between humans and chimps.

ERV's

From the very start I have offered ERV's as a simple and elegant example of the evidence that supports common ancestry between humans and chimps (and for all primates for that matter). I chose ERV's because they are unquestionably viral in origin. ERV's contain LTR's and a viral gene, such as env, gag, and pol. Some ERV's contain an entire viral genome, sometimes called a provirus. LTR's and MaLR's are also derived from viruses but they lack the viral genes that make ERV's unquestionably viral in origin. If MK wants me to include LTR's and MaLR's I will be happy to do so, but he will only have hundreds of thousands of more orthologous viral inserts to explain. I can't see how this is going to help MK's case.

So how does my argument support common ancestry? Because ERV's are viral in origin they came to part of the human and chimp genome through the process of random insertion, just as we observe viruses doing in today's world (see the table in my opening post). Therefore, when two individuals have the same retroviral insertion at the same spot in their DNA it is much, much more likely that they inherited that ERV from a common ancestor. The odds of even a single shared ERV at the same spot in the genome being due to two independent insertions are quite high. Those odds become astronomical when over 200,000 ERV's shared at the same spot in the genome are considered.

This is why MK wants to make the reader think that orthologous ERV's are in fact not orthologous (orthologous means shared at the same spot in the genome). But where has MK shown this? Nowhere. He argues that humans and chimps do not share 200,000 orthologous ERV's, but this conclusion is unavoidable. The chimp genome paper (which is linked at the bottom of the OP) lists very prominently the number of LINEAGE SPECIFIC ERV's. The important phrase here is "lineage specific". So how do scientists determine which ERV's are or are not lineage specific? It's actually quite simple. If they are not orthologous then they are lineage specific. Some ERV-K insertions are listed as human specific, some ERV-K insertions are listed as chimp specific, and other ERV-K insertions are orthologous. So this can't be a matter of retrovirus family specific insertions since one family of ERV's is listed as lineage specific in each lineage. Therefore, the list of lineage specific ERV's is a list of non-orthologous ERV's. How many are there? A trifling percentage of the nearly 200,000 ERV's found in humans. If MK wants to assert that these ERV's are non-orthologous then he needs to present evidence to support his claim.

MK also argues that the presence of PtERV's and CERV's in primates violates the nested hierarchy. What MK fails to mention is that these insertions are non-orthologous. The theory of evolution predicts that ORTHOLOGOUS ERV's should fall into a nested hierarchy, and they do. Non-orthologous ERV's are lineage specific insertions, those that are acquired after splitting from a common ancestor. The pattern of PtERV's and CERV's is exactly what the theory of evolution predicts for lineage specific insertions.

After the dust clears my original argument stands unrefuted. There are 200,000 human/chimp orthologous ERV's that can not be explained by indepenedent insertion and is best explained by common descent. PtERV's and CERV's in primates are non-orthologous and therefore do not violate the nested hierarchy predicted by the theory of evolution and common descent.

Conclusion

In conclusion, MK's criticisms of common descent do not amount to a challenge of the theory. Instead, they only serve to illustrate MK's own incredulity and misunderstanding of both logic and the evidence. MK at no point offers positive evidence for an alternate mechanism to explain the orthologous nature of ERV's, nor the nested hierarchy that ERV's create when all primates are considered. At no point does MK offer positive evidence for a mechanism that explains the differences between humans and chimps. MK argues that brain size doubled overnight between H. habilis and H. erectus. It didn't. MK argues that not knowing the genetic basis for human brain development falsifies common descent. It doesn't. MK argues that mutations in brain genes are deleterious. They aren't. MK argues that chimps and humans do not share 200,000 orthologous ERV's. They do. MK argues that the deleterious mutation rate is too high because of a 5% divergence. It's not. At every turn MK has been wrong, and continues to be wrong.

As for positive evidence for common ancestry, ERV's serve as 200,000 pieces of evidence. The pattern of shared ERV's is best explained by common ancestry. We observe this very process in humans every generation. Siblings will share 200,000 orthologous ERV's from birth, not because they were infected 200,000 times in the womb but because these sequences made their way into the genome through a common ancestor. If common ancestry is the obvious reason that humans share 200,000 orthologous ERV's then why isn't this the best explanation for orthologous ERV's found in humans and chimps. The obvious answer is that ERV's do evidence human and chimp common ancestry.

Before I finish, I would like to thank mark kennedy for putting in the effort to track down information in peer reviewed literature. This isn't always easy and it takes time, both of which mark has kindly shared with me in this debate. While I disagree with mark about evolution and common ancestry I have always appreciated his maturity, and would like to thank him again for being respectful even when there is obvious disagreements on the facts. Good luck mark, and many happy returns.

 

[mark kennedy]

Conclusion:​

First of all I would like to thank Loudmouth for agreeing to this debate. These debates are by their very nature contentious but he at least has the courage of his convictions. So with that on to my concluding remarks.

In conclusion, MK's criticisms of common descent do not amount to a challenge of the theory. Instead, they only serve to illustrate MK's own incredulity and misunderstanding of both logic and the evidence. MK at no point offers positive evidence for an alternate mechanism to explain the orthologous nature of ERV's, nor the nested hierarchy that ERV's create when all primates are considered. At no point does MK offer positive evidence for a mechanism that explains the differences between humans and chimps. MK argues that brain size doubled overnight between H. habilis and H. erectus. It didn't. MK argues that not knowing the genetic basis for human brain development falsifies common descent. It doesn't. MK argues that mutations in brain genes are deleterious. They aren't. MK argues that chimps and humans do not share 200,000 orthologous ERV's. They do. MK argues that the deleterious mutation rate is too high because of a 5% divergence. It's not. At every turn MK has been wrong, and continues to be wrong.

As for positive evidence for common ancestry, ERV's serve as 200,000 pieces of evidence. The pattern of shared ERV's is best explained by common ancestry. We observe this very process in humans every generation. Siblings will share 200,000 orthologous ERV's from birth, not because they were infected 200,000 times in the womb but because these sequences made their way into the genome through a common ancestor. If common ancestry is the obvious reason that humans share 200,000 orthologous ERV's then why isn't this the best explanation for orthologous ERV's found in humans and chimps. The obvious answer is that ERV's do evidence human and chimp common ancestry.

Before I finish, I would like to thank mark kennedy for putting in the effort to track down information in peer reviewed literature. This isn't always easy and it takes time, both of which mark has kindly shared with me in this debate. While I disagree with mark about evolution and common ancestry I have always appreciated his maturity, and would like to thank him again for being respectful even when there is obvious disagreements on the facts. Good luck mark, and many happy returns.

I have made the point repeatedly that ERVs are about 8% of the human genome. My opponent has repeatedly argued that it is not. He started out at 1% and eventually settled for 4% and some change. He is wrong:

Recently these problems have been lessened both by the systematic isolation of endogenous retroviruses from many different vertebrate taxa and by the generation of large amounts of sequence data by the Human Genome Mapping Project (HGMP) (7, 16, 32). As of December 1998, sequence information was available for over 10,000 BACs, or cosmids, representing approximately 235,000,000 bp, or 7% of the human genome (5)...The above criteria suggested the presence of 22 endogenous retroviral families within the 7% of the human genome that has been sequenced to date (Identification and Characterization of Novel Human Endogenous Retrovirus Families by Phylogenetic Screening of the Human Genome Mapping Project Database. J Virol. 2000 )

Endogenous retroviruses (ERVs) represent the proviral phase of exogenous retroviruses that have integrated into the germ line of their host (1). They typically consist of an internal region with three genes (gag, pol, and env) plus two flanking, noncoding LTRs, which are identical at the time of integration. Human ERVs (HERVs) comprise ≈5–8% of the human genome (2), with 98,000 elements and fragments (3), but phylogenetic analysis of conserved regions within their pol and env genes indicates that they form only a small number of clades among nonhuman exogenous and endogenous retroviruses (Long-term reinfection of the human genome by endogenous retroviruses. Proc Natl Acad Sci U S A. 2004)

Approximately 8% of the human genome is derived from retrovirus-like elements termed endogenous retroviruses (ERV) (14). Most of them are likely remnants of exogenous retrovirus infection of the germ line which became fixed in the population millions of years ago. (Human Endogenous Retrovirus Family HERV-K(HML-5): Status, Evolution, and Reconstruction of an Ancient Betaretrovirus in the Human Genome J Virol. 2004)

The human genome is littered by endogenous retrovirus sequences (HERVs), which constitute up to 8% of the total genomic sequence. The sequencing of the human (Homo sapiens) and chimpanzee (Pan troglodytes) genomes has facilitated the evolutionary study of ERVs and related sequences. (Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees. Journal of Virology, February 2006)

ENDOGENOUS retroviruses arise from retroviral infections of germ-line cells and subsequent incorporation into the host's genome (BOEKE and STOYE 1997). The human genome is estimated to contain tens of thousands of copies of human endogenous retroviruses (HERVs) and related sequences, accounting for ~8% of its sequence content (Human Endogenous Retroviral Elements as Indicators of Ectopic Recombination Events in the Primate Genome. Genetics, Vol. 171, 1183-1194, November 2005)​

How did he make such a glaring mistake? He misread the Human Genome Projects (HGP) paper, he based his argument on table 11 and made some very fundamental mistakes. Talk Origins said that ERVs make up 1% of the human genome. The HGP reported 4% and some change but the latest and greatest is telling us it's closer to 8%. The error is obvious and LM is oblivious.

The fossil evidence has one obvious flaw, where are the chimpanzee ancestors? The fact is that in order for us to have evolved from apes we would have to share a common ancestor with the chimpanzee that lived about 5 million years ago. When the two genomes were finally done they found the single base substitutions (actually differences) came to 35 million base pairs. That is pretty consistent with the mutation rate except there are another 5 million indels that come to 90 million base pairs and about 20 million base pairs from 8 chromosomal rearrangements. When the divergence goes from 1% to 5% doesn't the mutation rate go up with it, assuming a common ancestor of course. Check the peanut gallery, a Biologist was kind enough to provide the adjusted mutation rate. I would post it here but who is really going to believe me.

That comes to 5 single substitutions and 1 indel per year for 5 million years. That would be a mutation rate that would be a formula for extinction, not evolutionary adaptation. LM still won't admit that the indels are measured in base pairs. There is a very simple reason for that, he cannot reconcile the known mutation rate to the level of divergence.

That's not even my biggest problem with the common ancestor assumption. My problem is what about the deleterious affects that are always the result of mutations in highly conserved genes involved in the development of the human brain. How does this happen?

​

It just got bigger right? You can think that, you can argue that, you can insist on that but the proof is slowly coming in, highly conserved genes would have had to undergo a major overhaul with no known molecular mechanism. Here is just one example:

The 118-bp HAR1 region showed the most dramatically accelerated change (FDR-adjusted P , 0.0005), with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes (Supplementary Notes S3). Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (Myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400Myr ago. No paralogues were detected in any amniote genome draft. Resequencing in four primates further confirms that all 18 substitutions are very likely to have occurred in the human lineage. An RNA gene expressed during cortical development evolved rapidly in humans (Nature 14 September 2006)​

This is only one of the genes that would have had to be dramatically changed. This regulatory gene would have had to have 18 substitutions in a regulatory gene that has only had 2 since the Cambrian explosion. I don't really need an argument, the facts speak for themselves so evolutionists conflate and confuse the evidence with these melodramatic ad hominem arguments.

I have been told I should look at the SNPs involved in the regulatory gene. My response to this careless line of argumentation. Look at the affects!!!

This regulatory gene is located at chromosome 20q13.33. My opponent has said I should look into the SNPs, no problem, this is what I found:

Subtelomere FISH in 50 children with mental retardation and minor anomalies, identified by a checklist, detects 10 rearrangements including a de novo balanced translocation of chromosomes 17p13.3 and 20q13.33.

Am J Med Genet A. 2004

TP73 allelic expression in human brain and allele frequencies in Alzheimer's disease BMC Med Genet. 2004

Human brain derived neurotrophic factor (BDNF) genes, splicing patterns, and assessments of associations with substance abuse and Parkinson's Disease. Am J Med Genet B Neuropsychiatr Genet. 2005​

That's your argument? Alzheimer's and Parkinson's disease? That's not an argument that is the strongest argument against a common ancestor and the people who study this know it. This is not an isolated instance, follow this link and see what the known affects of mutations are on the human brain:

Human Genome Landmarks Poster: Chromosome Viewer

This is not a Creationist website, this is the Human Genome Project and it's funded by the Department of Energy. If you like the poster you can have a free copy. Pick a chromosome, any chromosome and look at the disease and disorder associated with mutations in these vitally important genes.

I have been feed bogus information since I started these debates and frankly I am sick of it. I challenged two of the commentators in our peanut gallery, both of them have made asinine arguments but refuse to defend them formally. One of them even intruded into a previous formal debate only to refuse a formal debate.

Just one more thing:

Abstract
Gene families are groups of homologous genes that are likely to have highly similar functions. Differences in family size due to lineage-specific gene duplication and gene loss may provide clues to the evolutionary forces that have shaped mammalian genomes. Here we analyze the gene families contained within the whole genomes of human, chimpanzee, mouse, rat, and dog. In total we find that more than half of the 9,990 families present in the mammalian common ancestor have either expanded or contracted along at least one lineage. Additionally, we find that a large number of families are completely lost from one or more mammalian genomes, and a similar number of gene families have arisen subsequent to the mammalian common ancestor. Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives.

The Evolution of Mammalian Gene Families. PLoS ONE. December 20, 2006​

Think what you like but I remain unconvinced that the a priori assumption of a common ancestor has anything to do with real world science. It is unnaturally imposed on science which is the secularists problem. When they try to push this off on the Christian faith they will be introduced into the wonderful world of Christian apologetics. I have quite an arsenal at my disposal, presuppostional apologetics works but my personal favorite is evidential apologetics. The most important factor is getting the facts straight so when the lie at the heart of the assumption of universal common ancestry finally shows itself you can strip the paper thin veiner away.

"For therein is the righteousness of God revealed from faith to faith: as it is written, The just shall live by faith. For the wrath of God is revealed from heaven against all ungodliness and unrighteousness of men, who hold the truth in unrighteousness; Because that which may be known of God is manifest in them; for God hath shewed it unto them. For the invisible things of him from the creation of the world are clearly seen, being understood by the things that are made, even his eternal power and Godhead; so that they are without excuse: Because that, when they knew God, they glorified him not as God, neither were thankful; but became vain in their imaginations, and their foolish heart was darkened. Professing themselves to be wise, they became fools, (Romans 1:17-22)​

 

[kiwimac]

Closed at request of Debate participants.