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In defense of Swamidass

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After reading Dr. Cornelius Hunter’s panning of Professor S. Joshua Swamidass’s recent article, Evidence and Evolution, I figured the professor must have written a truly awful piece. Nevertheless, I decided to go back and have a look at his article. And I’m very glad I did. Swamidass’s article was irenic in tone, easy to follow, deeply learned, and absolutely right.

Professor Swamidass’s olive branch

What Professor Swamidass was attempting to do in his article was to extend an olive branch to creationists. Nowhere in the article did he belittle or ridicule his opponents, and there was not a trace of the smug superiority which many scientists display, when talking to creationists. Indeed, he bent over backwards to be accommodating:

If we allow for God’s intervention in our history, it is possible we do not share a common ancestor with apes. Adding God into the picture, anything is possible…

Of course, adding God back into the picture, anything could have happened. An omnipotent God could have created us 6,000 years ago…

Of course, the scientific account is not the whole story. It is an open theological question how to complete the scientific account, and theological debate surrounding this question is important and engaging. One thing all should agree on; we humans are certainly more than just apes.

Nowhere in his article did Professor Swamidass argue that evolution is true, or that God made human beings via an evolutionary process. Instead, he attempted to show that the scientific evidence (taken on its own) supports human evolution, before concluding that if humans did not evolve, then theologians need to address this evidence:

Currently, it appears that, for some reason, God chose to create humans so that our genomes look as though we do, in fact, have a common ancestor with chimpanzees

It would have been very easy for God to design humans with genomes that were obviously different than apes, and clearly not a product of evolution. From some reason, He did not. He did not even make us as different from chimpanzees as mice are from rats. Why not?

Let me note for the record that young-earth creationist Todd Wood asked exactly the same question in a recent review of Fazale Rana and Hugh Ross’s revised 2015 edition of their book, Who Was Adam?:

Why do humans and chimps share such similar genomes, while the genomes of rats and mice differ so dramatically (see Mouse Genome Sequencing Consortium 2002)? What is the basis of the pattern of similarity (Wood 2006)?

…Similarity requires explanation, regardless of whether it’s similar genes or similar intergenic DNA.

Professor Swamidass draws no conclusions in his article; he merely poses a legitimate question which creationists have also wondered about. He certainly sounds like a very fair-minded man. I should add that Swamidass is a practicing Christian as well as a trained scientist. At the very least, his article warrants a courteous and carefully argued response. I regret to say that Dr. Hunter’s reply fails on this count: it is misinformed (as I’ll show below), polemical and curtly dismissive in tone, as the following extract shows:

The evolutionist has just made an unbeatable (and unfalsifiable) argument.

This is not science. Swamidass’ claim about what is and isn’t likely “without common descent” is not open to scientific scrutiny…

If Swamidass is correct then, yes, of course, the genomic data must be strong evidence for common ancestry. But it all hinges on his metaphysics. This is not about science. It never was.

Like that old baseball card, it’s just another worthless argument.

“Worthless argument”? Professor Swamidass deserves a better hearing than that.

Dr. Hunter’s criticisms of Professor Swamidass’s argument

Dr. Hunter’s failure to address the scientific evidence for common descent

Amazingly, Dr. Hunter manages to completely ignore the scientific evidence for evolution presented in Professor Swamidass’s article. Instead of addressing this evidence, he confines himself to quoting just two sentences from the article. Here’s the scientific evidence for human evolution, summarized by Swamidass, which Dr. Hunter overlooked:

In particular, be sure to check out the links to Dr. Dennis Venema’s more complete explanations of the evidence for the general public: common ancestry and genetic similarity (parts 1, 2, 3, and 4), synteny (parts 1 and 2), pseudogenes (parts 1 and 2), egg yolk (parts 1, 2, 3, and 4) and hominid evolution (hominid genetics and chromosome 2).

Evidence for human evolution: we have remnants of genes for making egg yolks

Here’s just one intriguing piece of evidence for common ancestry, which Dr. Dennis Venema writes about in a series of articles linked to by Professor Swamidass. Unfortunately, this evidence is never even mentioned by Dr. Hunter in his article:

Vitellogenins are large proteins used by egg-laying organisms to provide a store of nutrition to their embryos in egg yolk. Since vitellogenins are so large, they are a good source of amino acids when digested (proteins are made of amino acids linked together). Many of the amino acids in vitellogenins have sugars attached to them as well, so they also serve as a source of carbohydrates. The three-dimensional shape of vitellogenin proteins also acts as a carrier for lipids. As such, vitellogenins can be synthesized in the mother and transferred to the yolk as a ready-made supply of amino acids, sugars, and lipids for the developing embryo.

Placental mammals, on the other hand, use a different strategy for nourishing their embryos during development: the placenta. This connection between the mother and embryo allows for nutrient transfer right up until birth. As such, there is no need for vitellogenins, or storing up a supply in the egg yolk for the embryo to use. Evolutionary biology predicts that placental mammals descend from egg-laying ancestors, however – and one good line of evidence in support of that hypothesis (among many) is that placental mammals, humans included, have the remains of vitellogenin gene sequences in their genomes.

Dr. Hunter: we can’t say what God would or wouldn’t do

Dr. Hunter’s response to such arguments is to cry foul, on the grounds that such an argument involves an appeal to metaphysics:

A scientist cannot know that something is unlikely “without” his theory. That implies knowledge of all other possible theories. And that knowledge does not come from science.

I disagree. The scientific case for human evolution doesn’t need to specify what a Designer would or wouldn’t do. All it says is that if the Designer of life has no special reason to make X, and we discover X, then X should count as a surprising fact – and hence, a prima facie improbable one. On a special creationist account of human origins, there is absolutely no reason to expect that humans would have what appear to be the remains of genes used for making egg yolks in their DNA – just as there is no particular reason to expect that humans would be more genetically similar to chimps than rats are to mice – or for that matter, than foxes are to wolves, or horses are to donkeys. And let’s remember that most creationists consider horses and donkeys to be members of the same “kind,” just as they consider foxes and wolves to be members of the same kind, and of course, rats and mice as well (see here for a detailed discussion of kinds by Dr. Jean Lightner, from Answers in Genesis. Reasoning on Bayesian grounds, these striking and singular facts have a high probability on the hypothesis of common descent, but are surprising (and hence improbable) on a hypothesis of separate creation. One can only conclude that these facts lend scientific support to the hypothesis of common descent.

Can evolution account for the fact that humans and chimps are genetically much more similar than mice and rats?

Dr. Hunter also faults Professor Swamidass for claiming that the similarity of human and chimpanzee genomes was “predicted by common ancestry,” and that the recent scientific discovery that “humans are about 10 times more genetically similar to chimpanzees than mice are to rats” was “just as predicted by the fossil record.” Hunter replies:

First, the high chimp-human genomic similarity was not predicted by common ancestry. No such prediction was made and no such prediction is required by common ancestry. Common ancestry would be just fine with very different levels of similarity than 98-99%…

Second, Swamidass’ claim that mouse-rat divergence, compared with the chimp-human divergence, is “just as predicted by the fossil record” is also blatantly false…

In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome.

What Dr. Hunter omits to mention is that Professor Swamidass attached a lengthy footnote, which supplies the context for his remarks about rats and mice:

A common lawyerly objection to this evidence is that these similarities are “equally” explained by common “design.” As scientists, our response to this objection is data. Many modern creationists think that the genetic evidence shows that mice and rats share a common ancestor, even though they are 10 times less similar than humans are to chimpanzees. Starting from the genetic evidence, why is it hard to believe chimpanzees and humans are related (less than 1.5% codons different), when we readily accept mice and rats are related (more than 15% different)? Of course, on the outside, not looking at our genomes, humans are very different than chimpanzees, much more different than mice are from rats. Common ancestry predicts this discrepancy between function and genetics by recognizing that genomes are better explained by evolutionary history than readily observable differences between species; mice and rats are more different because they changed more quickly (because of their shorter generation time) for a longer period of time than humans and chimpanzees. What design principle can explain why humans are 10 times more similar to chimpanzees than mice are to rats? No one knows.

While Dr. Hunter is correct in pointing out that the hypothesis of that humans and chimps shared a common ancestor, taken by itself, implies nothing about their degree of genetic similarity, he neglects to mention that scientists routinely make use of molecular clocks in order to determine when two species (A and B) diverged, based on their degree of genetic similarity. They do this by using the fossil record to determine independently when two other species (X and Y) diverged, and comparing the divergence between X and Y with that between A and B, in order to calculate the date when species A and B diverged. The basic idea here is that nucleotide sequences in DNA change over time at a rate which is roughly constant across all species, as predicted by Motoo Kimura’s neutral theory of evolution, which, as Professor P.Z. Myers explains in a 2014 blog post, has been vindicated over “selectionist” theories (which categorized mutations as either advantageous or disadvantageous) by the experimental evidence:

First thing you have to know: the revolution is over. Neutral and nearly neutral theory won. The neutral theory states that most of the variation found in evolutionary lineages is a product of random genetic drift. Nearly neutral theory is an expansion of that idea that basically says that even slightly advantageous or deleterious mutations will escape selection — they’ll be overwhelmed by effects dependent on population size. This does not in any way imply that selection is unimportant, but only that most molecular differences will not be a product of adaptive, selective changes…

When comparing the rates of change between homologous genes in different species, we had a bit of a surprise: they are very roughly, sloppily constant. That shouldn’t be true under pure selection theory, but it turns out to make a lot of sense under nearly neutral theory. There is a tradeoff in the rate of mutations occurring, and in becoming fixed in a population. A very large population size will accumulate more mutations purely by chance, but the probability of a single mutation becoming fixed in the population is reduced under large population sizes. When you do the math, you discover that population size cancels out, and the frequency of novel forms becoming fixed over time is dependent solely on the mutation rate.

Think about that. If you compare two species, the number of nucleotide differences between them is basically going to be simply the mutation rate times the number of generations separating them from their last common ancestor. That’s how we can use a molecular clock to date the time of divergence of two lineages.

Professor Soojin Yi (School of Biology, Georgia Institute of Technology, Atlanta) provides a helpful summary of how scientists use molecular clocks and what their limitations are, in a recent article titled “Neutrality and Molecular Clocks,” (Nature Education Knowledge 4(2):3, 2013).

So, what do the fossils show? Sahelanthropus (pictured at the top of this post), who lived around 7 million years ago, is currently considered to be very close to the last common ancestor of humans and chimpanzees (see this family tree for a summary of changes which are believed to have occurred in the human lineage). By contrast, rats and mice appear in the fossil record at least 14 million years ago, according to the Wikipedia article on Murinae (the subfamily comprising Old World rats and mice):

The first known appearance of the Murinae in the fossil record is about 14 million years ago with the fossil genus Antemus. Antemus is thought to derive directly from Potwarmus, which has a more primitive tooth pattern. Likewise, two genera, Progonomys and Karnimata, are thought to derive directly from Antemus. Progonomys is thought to be the ancestor of Mus [the common mouse – VJT] and relatives, while Karnimata is thought to lead to Rattus [the rat] and relatives. All of these fossils are found in the well-preserved and easily dated Siwalik fossil beds of Pakistan.

For more information on the evolution of rats and mice, see here.

Is the chimpanzee really the animal closest to us?

Left: A chimpanzee mother and baby, Baltimore Zoo. Cropped image, courtesy of Wikipedia.
Right: Orangutan, Semenggok Forest Reserve, Sarawak, Borneo, Malaysia. Courtesy of Wikipedia.

Dr. Hunter’s discussion of the difficulties attending the hypothesis of human evolution is even more disappointing. He begins by attacking the claim that the chimpanzee is the creature closest to human beings:

Evolutionists believe that we humans evolved from a small ape-like creature and that our closest relative on the evolutionary tree is the chimpanzee. The chimpanzee must be our closest relative, they reason, because the chimp’s genome is closest to ours, and according to evolution, genetic mutations are the fuel behind evolutionary change.

The problem with this reasoning is that the chimpanzee is not very similar to humans according to many other measures. There are enormous differences between the two species. Furthermore, in its morphology and behavior, the orangutan is closer to humans than the chimpanzee.

A quick point about the genetic similarities between humans and chimp DNA: they really are about 98% similar, as I argued in a post last year. What’s more, even alleged de novo genes found in human beings turn out to have 98% similar counterparts in chimps.

As regards Dr. Hunter’s claim that humans are morphologically more like orangutans than chimpanzees, I’m afraid he’s relying on out-of-date information here. Back in 2009, Professor Jeffrey Schwartz and Dr. John Grehan generated a brief flurry of controversy in the scientific world when they published a paper which listed 63 physical characteristics which had been verified as unique to humans and other great apes – chimps, gorillas, and orangutans – and discovered that humans shared no less than 28 of these characteristics with orangutans, but that they only shared two characteristics with chimpanzees, seven with gorillas, and seven with all three apes (chimpanzees, gorillas, and orangutans). Dr. Schwartz has long argued that our closest relative is the orangutan (from whom he says we diverged 12 or 13 million years ago), and he contends that the genetic data don’t tell the whole story, because most human-chimp comparisons only look at the coding region of the human genome. However, in 2010, another team of researchers (Lehtonen et al.) redid the research, using a much larger set of 300 anatomical features, and found (with a 98% degree of confidence) that the ape most similar to human beings was the chimpanzee, after all. Grehand and Schwartz hit back with a paper of their own in 2011, in which they argued that Lehtonen et al. shouldn’t have counted some of the anatomical features listed in their study, but Lehtonen et al. replied with an article showing that Grehan and Schwartz were guilty of logical inconsistencies in their methodology. In other words: evidence purporting to show that humans are physically more like orangutans than chimpanzees turned out to be highly questionable, and there’s no good reason to doubt that chimpanzees are the apes which are closest to human beings – although recent evidence suggests that the common ancestor of humans and chimps may have walked like an orangutan. However, I don’t blame Dr. Hunter for accepting the claim that humans are anatomically closer to orangutans than to chimps: at one point, I was taken in by it myself.

If even the evolution of proteins requires a Designer, how much more so does human evolution

Dr. Hunter continues:

According to evolution, you can’t have mutations occurring for some purpose, such as creating a design. And natural selection doesn’t help — it cannot induce or coax the right mutations to occur. This makes the evolution of even a single protein, let alone humans, statistically impossible.

In this passage, Dr. Hunter is alluding to the pioneering work of Dr. Douglas Axe, the author of the 2010 paper, The Case Against a Darwinian Origin of Protein Folds, which I blogged about here. See also here, here and here for follow-up comments by Dr. Axe and Dr. Ann Gauger, in response to criticisms. As far as I can judge, evolutionists have failed to mount a substantial challenge to Dr. Axe’s arguments demonstrating the astronomical improbability of certain protein folds which are essential for all living organisms having evolved by unguided processes. So I am in complete agreement with Dr. Hunter that human beings did not get here by either a chance process or by natural selection.

However, Professor Swamidass never claims in his article that human beings originated via a blind process. As I mentioned above, he’s a scientist who is a Christian. His sole aim, in writing the article, was to show creationists that there is a wealth of scientific evidence supporting the claim that human beings and chimpanzees shared a common ancestor. Nothing in that claim stipulates the mechanism whereby humans arose: it may have been a guided process or an unguided one.

The mystery of human consciousness

Next, Dr. Hunter argues that evolution cannot account for the mystery of human consciousness:

The incredible designs in the human body are not the only thing those random mutations have to create—they will also have to create human consciousness.

Evolutionists may try to explain consciousness as an “emergent” property that just luckily arose when our brain somehow evolved. Or they may try to explain that consciousness is really no more than an illusion. But these are just more demonstrations of anti-realism in evolutionary thought. Evolutionary theory constructs mechanisms and explanations that do not correspond to the real world. So this is another problem Swamidass will need to overcome.

However, nowhere in his article does Professor Swamidass attempt to argue that evolution can explain human consciousness. All he is endeavoring to demonstrate is that there is strong scientific evidence that humans and chimps had a common ancestor. Remember: the guy is a Christian, not an atheistic reductionist.

Can the relatively tiny modifications of an ape-like ancestor’s genome account for the vast differences between humans and chimps?

Dr. Hunter ridicules the notion that the morphological differences between humans and chimps can be explained by a relatively small number of modifications in their ancestors’genomes, when species that have undergone much greater genetic modification display far fewer morphological differences:

In recent decades the genomes of humans and chimps have been determined, and they make no sense on evolution. One of the main problems is that the genes of the two species are almost identical. They are only about 1-2% different and, if you’re an evolutionist, this means you have to believe that the evolution of humans from a small, primitive, ape-like creature was caused by only a tiny modification of the genome.

This goes against everything we have learned about genetics. You can insert far greater genetic changes with far less change arising as a consequence. It makes little sense that tiny genetic changes could cause such enormous design changes to occur.

Dr. Hunter’s argument is flawed, because he overlooks the fact that the vast majority of genetic changes are now known to be either neutral or nearly neutral, as explained above: they are product of random genetic drift, and they are mostly non-adaptive. By contrast, morphological changes (including the “design changes” referred to by Dr. Hunter) are often subject to natural selection, which means that they may be either beneficial or deleterious. Consequently, the degree of genetic divergence between two species tells us little or nothing about how different they are, morphologically. That explains how the morphological differences between rats and mice can be relatively slight, even though rats and mice are believed to have diverged long before humans and chimps (which are so morphologically dissimilar that they were placed in separate families until scientists discovered how similar they were genetically).

It has been calculated (Arbiza, 2006; Yu 2006; Donaldson & Gottgens 2006; Kehrer-Sawatzki & Cooper 2007) that a mere 340 beneficial mutations would have been sufficient to transform the common ancestor of man and chimp into a human being, according to biologist Ian Musgrave of Panda’s Thumb. (That’s 240 mutations in protein-coding genes and 100 in regulatory genes.) By contrast, the number of (mostly neutral) mutations occurring in the human lineage is thought to have been about 22.5 million. In other words, the neutral mutations in our lineage outnumber the beneficial mutations by about 100,000 to 1. The vast majority of genetic differences between humans and chimpanzees have nothing to do with survival, or evolutionary fitness.

Could 340 beneficial mutations have been enough to make us human?

Dr. Hunter is aware of this argument, but he doesn’t find it convincing:

Not only is evolution limited to tiny genetic modifications to create the human, but the majority of those modifications would have had to be of little or no consequence…

…[The authors of a 2005 paper on the chimpanzee-human genome comparisons] were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”

That’s right. According to current evolutionary thinking, most of the mutations separating us from chimps were inconsequential, from a survival perspective. A relatively small number of changes – in fact, a mere 340 – made all the difference.

Now, you might be inclined to say: “That’s ridiculous!” Fine. My response is: prove it. You can’t just rely on intuition, because intuition is not infallible. To illustrate my point, consider a transition which dwarfs even the metamorphosis from an ape-like creature to a human being: the transformation from a land animal to a whale. Ask yourself: how many steps would have been required to accomplish this change? Biochemist Larry Moran has an answer for you: “Evolutionary biologists who have spent their entire careers studying evolution, genetics, and developmental biology are comfortable with a few thousand mutations causing the transformation from land animals to whales.” Crazy? That’s what I thought too, when I saw the figure. But if you do the calculations, it turns out that a few thousand mutations might be enough after all, for reasons I discussed in a recent post.

Is there any evidence for natural selection operating on the human brain?

Next, Dr. Hunter argues that the only evidence for natural selection in the human genome relates to relatively trivial functions like smell and hearing, and that there’s no evidence for natural selection operating on the human brain:

When evolutionists search for genes in the human genome that do show signs of selection, rather than neutral drift (again, under the assumption of evolution), they find only a limited repertoire of functionality. For example, one study found genes involved in the sense of smell, in digestion, in hairiness and in hearing. In other words, evolution is suggesting that we differ from the chimp mainly in those functions. It is a silly conclusion and another problem for Swamidass to explain.

Dr. Hunter neglects to inform his readers that the study he cited is a very old one: it goes back to 2003. What’s more, the study included an important disclaimer: “This study has focused only on protein-coding genes, and it will require examination of regulatory sequences to determine the contribution of regulation of gene expression to the evolutionary divergence between humans and chimps.” A more recent paper by Capra et al., published in the Philosophical Transactions of the Royal Society B in 2013, reveals that out of the 2649 non-coding human accelerated regions (ncHARs) which they analyzed in the human genome, about 30% (or 773) function as developmental enhancers, and that using a prediction tool known as EnhancerFinder, the scientists predicted that “251 of the 773 ncHAR enhancer candidates are active in brain development, 194 are active in limb development and 39 are active in heart development.” It turned out that among the validated enhancers, brain enhancers were actually the most common. So much for Dr. Hunter’s claim that the functions identified by scientists in which humans differ from chimps mainly relate to the sense of smell, digestion, hairiness and hearing.

A molecular clock that ticks at different rates in different regions of the human genome

But Dr. Hunter has more up his sleeve. This time, he quotes from a paper dating back to 2005, which found that nucleotide divergence rates are not constant across the human genome. In other words, the molecular clock ticks at a different rate at different places:

That 2005 paper also found a host of chimp-human comparisons that are nonsensical on evolution… For example, if you look at large segments of DNA, which are corresponding in the human and the chimp, you find unexplainable variations in the chimp-human differences…The usual explanatory devices do not work, so evolutionists are left only with the claim that local variations in the mutation rate did it—which amounts to special pleading…

Hang on a minute. How big are the differences we’re talking about here? Are we talking about a ten-fold difference between divergence rates across the genome? Nope. Not even close. A five-fold difference, perhaps? Wrong again. To see what Dr. Hunter is talking about, take a look at this graph. It shows that the overall difference between human and chimp DNA is about 1.2%. If we compare different chromosomes, we find that the difference is slightly higher on some chromosomes than others. And that’s all. If we look at the median figures for chromosome pairs 1 to 22, we find that the genetic difference between humans and chimps varies from about 1.1% to a little under 1.4%. The authors were a little surprised that there was even that much variation, and they wrote: “The average divergence in 1-Mb segments [of the genome – VJT] fluctuates with a standard deviation of 0.25%, which is much greater than the 0.02% expected assuming a uniform divergence rate.” To recap: the study’s authors reported that the mean divergence between human and chimp DNA is 1.2%, and if the molecular clock ticked at a uniform rate across the genome, then the authors would have expected relatively slight variations in this divergence. Instead, they found fluctuations with a standard deviation of 0.25%, which is still insignificant compared to the mean divergence of 1.2%. In other words: so what? Dr. Hunter is making a mountain out of a molehill.

Local variations in the genetic divergence rate between humans and chimps

Dr. Hunter continues:

The supposed divergence rate between chimps and humans not only has an unexplainable variation in large, 1-Mb segments of DNA, it also has an unexplainable variation towards the ends of most chromosomes. This is another problem that seems to make no sense on evolution, which Swamidass must explain.

But that’s not all.

This supposed divergence rate between chimps and humans also has an unexplainable variation that correlates with chromosomal banding. Again, this makes no sense on evolution. Why should the chimp-human divergence vary with the banding pattern? Evolutionists have only just-so stories to imagine why this would have happened, and it is another problem for Swamidass to address.

So, how much of a variation are we talking about here? If we look at the graph provided by the authors of the study, we see that even near telomeres (the ends of chromosomes), the level of divergence between human and chimp DNA never gets above 2.1%, and elsewhere in the genome, it never falls below 1.0%. In other words, we’re talking about a two-fold variation in the rate at which the molecular clock ticks, in the worst possible case. Earth-shattering, isn’t it?

Dr. Hunter wonders why the level of chimp-human genetic divergence would vary with the chromosomal banding pattern, and why it would be higher near the ends of chromosomes, if humans evolved. Short answer: I don’t know, and neither do the study’s authors. But I’d like to ask Dr. Hunter a question: can he account for these facts, on a creationist account of origins? He can’t. In other words, what we have is a curious fact which neither evolution nor creation explains well, and which is fatal to neither theory – or putting it more succinctly, much ado about nothing.

Can evolution account for the dissimilarities in rat and mouse genomes?

But Dr. Hunter thinks he has another ace up his sleeve: the fact that the genetic difference between mice and rats is about 10 times greater than that between humans and chimps.

This supposed divergence rate between chimps and humans is not consistent with the supposed divergence rate between the mouse and rat. The mouse-rat divergence is about an order of magnitude greater than the chimp-human divergence. And yet the mouse and rat are much more similar than the chimp and human. It makes no sense on evolution. In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome…

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

Dr. Hunter is right on one point: scientists were at first surprised to discover that the genetic difference between rats and mice was so large. That’s because they based their prediction on the morphological differences between rats and mice, which are relatively small, and inferred that the genetic difference would be small, too. That was a big mistake, for reasons explained above: the vast majority of the genetic differences between any two species are neutral or near-neutral mutations, which dwarf beneficial mutations by a factor of about 100,000 to 1. However, the fossils tell a different story: rats and mice diverged at least 14 million years ago, compared with 6 or 7 million years for humans and chimps. And when scientists calculate the time of divergence using genetic differences, they arrive at a median figure of 17.9 million years ago for the date when rats and mice diverged, versus 6.2 million years ago for the split between humans and chimps, according to timetree.org. I’d say that tallies reasonably well with the fossil record. And I don’t say that lightly: I have in the past been highly critical of inconsistencies in the molecular clock, which I highlighted in a post written four years ago. There is still a lot we don’t know, and alert readers will have noticed that current estimates of the date when humans and chimps diverged vary considerably, as this graph reveals. Nevertheless, the vast majority of the estimates lie between four and nine million years ago, so we’re talking about a two-fold variation, which is still far less than even one order of magnitude. That’s annoying, but scientists can live with it, just as astronomers back in the 1970s and 1980s were able to live with the fact that the age of the universe lay somewhere between 10 and 20 billion years, depending on the method you used to measure it. (They’ve now concluded that it’s 13.8 billion years old.)

Dr. Hunter’s last stand

But Dr. Hunter believes he has one more argument that will demolish the case for human evolution:

The mouse-rat divergence date is estimated by evolutionists to be older than the chimp-human divergence date. Furthermore, the lifespan and generation time for mice and rats are much shorter than for chimps and humans. From this perspective, and given these two effects, one would conclude that the mouse-rat genetic divergence should be much greater—at least two orders of magnitude greater—than the chimp-human genetic divergence. But it isn’t. It is only about one order of magnitude greater.

Wrong. As we’ve seen, mice and rats diverged around 18 million years ago, compared with around six million years ago for humans and chimps. That’s a three-fold difference. What about the effects of generation time on the molecular clock? Soojin Yi addresses this point in her 2013 paper, “Neutrality and Molecular Clocks,” which I cited above:

Wu & Li (1985) were the first to test the generation-time effect hypothesis using DNA sequence data. They used data from 11 genes of primates and rodents. Since primates have a much longer generation time than rodents do, the molecular clock should be faster in rodents compared to primates. Indeed, they found that for synonymous sites, rodents show approximately two times the rate of molecular evolution when compared to primates (Wu & Li 1985). For nonsynonymous sites however, such an effect was not found. In other words, the neutral molecular clock, but not the amino acid molecular clock, ticks faster in the rodent lineage compared to the primate lineage, which fits well with the idea of a generation-time effect.

So the neutral molecular clock ticks twice as fast for rats and mice as it does for primates. Multiply that by the three-fold difference between the 18-million-year-old mouse-rat divergence date estimated by evolutionists and the 6-million-year-old human-chimp divergence date, and you get an expected level of genetic divergence which is just six times greater – and not two orders of magnitude (or 100 times) greater, as calculated by Dr. Hunter. This figure of a six-fold difference comports well with the ten-fold genetic divergence reported by Professor Swamidass in footnote 2 of his article: at least 15% of the codons in rats and mice are different, compared with less than 1.5% in humans and chimps.

Conclusion

There is a lot that we still don’t know about human origins. I accept that. But it would be foolish to deny that the scientific evidence points clearly to our having shared a common ancestor with the chimpanzee. Such a conclusion is in no way at odds with Intelligent Design.

What do readers think?

UPDATE:

Readers may wish to peruse the following articles, written in response to my post and to Professor Swamidass’s article, “Evidence and Evolution”:

A Response to VJTorley by Dr. Cornelius Hunter.
One Long Argument — Responding to VJ Torley on Human-Ape Common Descent by Dr. Cornelius Hunter.
Of Tree Rings and Humans by David Klinghoffer.
Debating Common Ancestry by John West.

Professor Swamidass has also written a follow-up article:
Call for Response to the Tree.

I also wrote a short comment in response to Professor Swamidass’s article, “Evidence for Evolution”, which has recently been updated with an FAQ section:

Hi Dr. Swamidass,

Thank you very much for your kind remarks about my post on Uncommon Descent.

I’d just like to comment briefly on what you said about Dr. Hunter in the FAQ:

“Third, I do believe that Dr. Hunter is not being intentionally deceptive or manipulative. I believe he is making a good faith effort, to the best of his abilities, to engage the evidence I have raised.”

I would like to endorse what you said. I pulled no punches in my post, and on a few occasions, I did criticize Dr. Hunter for relying on flawed arguments. I also wrote that he “neglects to inform” his readers on a couple of basic points. For the record, I wish to make it quite clear that I am not accusing Dr. Hunter of being intentionally deceptive. All of us are, at times, guilty of an unintentional bias towards arguments that we personally favor, and it is all too easy to ignore what we might perceive as very minor or trivial problems in these arguments, when presenting them to an audience. That was what I had in mind when I wrote about Dr. Hunter’s “neglect.”

Despite my differences with Dr. Hunter, I have the greatest respect for him as a Christian, and I would like to thank him for his forbearance and courtesy.

Likewise, when I referred to Dr. Hunter in my post as believing he had an ace up his sleeve, I was not implying that he was resorting to any sleight-of-hand or trickery. Rather, I was using the term in the sense in which the Cambridge English dictionary defines it: secret knowledge or a secret skill that will give you an advantage.

For the record, I believe Dr. Hunter to be an honest man. And I apologize for any pain or distress suffered by Dr. Hunter as a result of reading my post. I wish him well.

Comments
Hi Eric Anderson, You ask: "Do you seriously think 340 beneficial mutations in DNA could turn an ape-like creature into a human, and 3000 beneficial mutations in DNA could turn a land animal into a whale?" I have to say (reluctantly) that I haven't seen any rigorous quantitative argument yet as to why this could not be the case. I attempted to provide one in an earlier post at https://uncommondescent.com/intelligent-design/are-3000-beneficial-mutations-enough-to-transform-a-land-animal-into-a-whale/ and I was forced to concede that "the Darwinian scenario for whale evolution won’t be overturned simply by calculating the number of morphological and physiological changes that would have been required." I also wrote that if 100 organs (or systems) in the whale underwent transformation, and if “only” 30 mutations per organ were required during the evolution of the whale, then we would obtain a total of 3,000 (= 30 x 100), which more or less agrees with Professor Larry Moran’s estimate of a few thousand mutations. For human evolution, I'm guessing that 30 to 50 separate organs (or systems) underwent transformation, and that there were 10 mutations per organ, with these mutations occurring more or less in sync (due to intelligent guidance), making 300 to 500 mutations. But I could be wrong, of course.vjtorley
May 16, 2016
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Jerry gpuccio VJT This article by Richard Sternberg is also very interesting and relevant. https://shar.es/1dWBZAbill cole
May 16, 2016
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Jerry gpuccio VJT http://bit.ly/1TfR5Ha Although I have had time to only skim, this paper is very interesting. An important read for everyone. VJT: it would be great to get Joshua's detailed thoughts. gpuccio: your thoughts would greatly appreciated.bill cole
May 16, 2016
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thanks for your answers gpuccio. i will focus now in my main a rgument (also because of my english limitation i try to make it short). you said: "However, the fact remains that most known genetic diseases are associated to non synonymous mutations."- true. but again- we cant know if most of the synonymous codons have some function or not. we know for sure that there is some meaning for some of them. maybe even for all of them. it will change the whole picture. even if synonymous mutation doesnt make a diseases it dioesnt mean that it doesnt have a function. you said: "Yes. You have to get the nucleotide sequence of the two genes in the two (or more) species). It must be strictly the coding sequence. Then you have to align the two sequences. "- the problem is that you need to assume that those species evolved from a commondescent (and therefore you c an know how the originial sequence look like). so we need to assume first that evolution is true. or you talking about species from the same kind?(family) by the way gpuccio, what do you think about ic systems? i think that its a very s trong argument against a commondescent. it will be interesting to discuss about it. i have some interesting points.mk
May 16, 2016
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Eric,
Do you seriously think 340 beneficial mutations in DNA could turn an ape-like creature into a human
From what I understand it is tens of thousands of differences. I suggest you read the Wilcox paper I reference to above. The differences are not in the protein coding regions but in control mechanisms. We should stop talking about the human and chimp genomes in terms of similarity and differences in the coding regions and start talking about the real differences between the two species. The coding region comparison is a red herring. http://bit.ly/1TfR5Hajerry
May 16, 2016
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VJT: I'm sorry to come back to this, but I really have to ask: Do you seriously think 340 beneficial mutations in DNA could turn an ape-like creature into a human, and 3000 beneficial mutations in DNA could turn a land animal into a whale?Eric Anderson
May 16, 2016
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gpuccio VJ eric all
The only important point which is more in favor of universal descent with designed modifications is that the greatest part of basic protein information (IOWs protein superfamilies) is already present in LUCA or appears during the further differentiation of prokaryotes, and a lot of that existing information is re-used in eukaryotes, and therefore in metazoa. The explosion of multicellular beings, too, is vastly based on molecular tools which are already present in single celled eukaryotes. At each stage, however, a lot of new original information appears. That’s what I can say. Future data will certainly help to reason better about these issues, as a true biological science based on the acceptance of design principles emerges.
I completely agree with this:-) I look forward to working with everyone to help put this fascinating puzzle together.bill cole
May 16, 2016
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I have a question.
Are there any other organisms/species besides humans that developed primarily by control mechanisms and not by differences in coding regions?
I am sure there are some with minor differences due to control regions but none as massive as humans are from any other primates. It is apparent that the main difference between humans and chimps in not due to protein coding regions but to differences in control of which proteins get expressed. These differences are massive while the differences in coding regions are small. How did these control regions arise? I don't see how mutations etc could have done it without creating numerous sub populations with and without the various changes in control mechanisms. So are humans the only species (and thus unique), that arose due to the differences between it and other species due to developments in the coding regions. The question is why are humans unique and this is the real question that all of evolutionary biology is missing. We are so focused on variation in coding regions as the source of species differences while for humans this is minimal while the differences in control regions are massive.jerry
May 16, 2016
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Origenes: "Do you hold that — with the exception of the first organism — all species/information/sequences are introduced by CD? Are e.g. the Cambrian animals introduced by CD?" Very good question! I really don't know, and probably we have not enough data to decide, at present. That's what I mean when I say that CD needs not be universal. As I see it, the available facts on which we can reason are: 1) While each complex functional transition (for example one new functional protein) can in general justify a design inference, there are a few events in natural history which are true "avalanches" of new functional complexity. They are essentially: a) OOL b) Eukaryogenesis c) The appearance of metazoa d) The rather sudden appearance of practically all basic body plans (Cambrian Explosion) Where c and d could be almost contemporaries, or slightly distant in time, according to the different views. There are certainly other examples. The Ediacaran explosion is very interesting and highly controversial, for example. The flowering plants explosion could be another example. Now, a theory of universal CD would be that, while OOL could have been a special event of very massive design implementation "from scratch" (which is my hypothesis that LUCA was also FUCA), the rest of design implementation was realized through descent with designed modifications. That is certainly possible. But it is also possible that, at least in the massive events of eukaryogenesis and/or metazoa development and body plan generation, the process could have been different again, for example multicentric and with components "from scratch". The only important point which is more in favor of universal descent with designed modifications is that the greatest part of basic protein information (IOWs protein superfamilies) is already present in LUCA or appears during the further differentiation of prokaryotes, and a lot of that existing information is re-used in eukaryotes, and therefore in metazoa. The explosion of multicellular beings, too, is vastly based on molecular tools which are already present in single celled eukaryotes. At each stage, however, a lot of new original information appears. That's what I can say. Future data will certainly help to reason better about these issues, as a true biological science based on the acceptance of design principles emerges.gpuccio
May 16, 2016
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Eric Anderson: "Keen minds running in the same vein and all that . . ." Indeed! :) So be it: Descent with designed modifications!gpuccio
May 16, 2016
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Eric Anderson: "Yet none of these engineering and logical constraints slow the Darwinist imagination one whit. Chance did it. Luck rules the day." I know, I know... :)gpuccio
May 16, 2016
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VJ at #115: "I may be wrong, but as far as I can tell, the calculation for the number of neutral mutations in the human line makes no assumptions regarding design. The number is calculated using the postulates of the neutral theory. If you can show me where the calculations assume no design, then of course, I’m open to changing my mind." The calculation assume no design, exactly because they are made using the postulates of the neutral theory, which does no consider design as a possible source of variation. If we consider the possibility of design interventions, everything changes. Indeed, any designed variation which takes place in parts of the genome whose function we don't understand (especially regulatory parts) would be conflated with neutral variation in the classical neutral theory. Neutral theory can be more or less correct in explaining how true neutral random mutations can accrue, but certainly it cannot tell us anything about how many designed variations are present in a genome. For protein coding genes, we can have an idea of the introduction of new functional information looking at the appearance of new genes, or at the modifications of existing genes. But, in the apes-to-humans transition, we already know that the role of protein coding genes is limited, and that most of the difference must be related to different epigenetic regulations. Therefore, the design interventions which implemented the transition will be conflated with neutral variation, if we just apply the neutral theory.gpuccio
May 16, 2016
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mk: Your final question: "4)you said: “Ka/Ks is a measure that is done on existing protein coding genes, comparing their nucleotide sequence.”- can you explain how? thanks." Yes. You have to get the nucleotide sequence of the two genes in the two (or more) species). It must be strictly the coding sequence. Then you have to align the two sequences. I do that with Clustal, a specific software. Then you import the alignment into some software which can compute Ka/Ks. I use the R module seqinR. This kind of software uses a rather complex algorithm, which evaluates sites in the sequence which are potentially "synonymous" or "non synonymous", according to the potential effects of variation in that site. Then the rate of variation between the two sequences in non synonymous (Ka) and synonymous (Ks) sites is counted, and finally the rate of the two rates is the Ka/Ks. For a simple summary, here is the Wikipedia page about the subject.gpuccio
May 16, 2016
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mk at #110: "about point 1)if the protein sequence havent realy changed (in the dna level)during one bilion years, then we can conclude that most of the mutations in this gene arent neutral. even for synonimous codons. do you agree with this conclusion?" But the sequences do change at DNS level, because synonymous mutations can be observed there. If you look at my computation of Ka/Ks for histone H3, you can see that the rate of synonymous mutations is about 100 times greater than the rate of non synonymous, in a protein coding gene which is extremely conserved at the level of AA sequence. That is exactly the important point. 2)do you have a reference that those exmaples are rare and not common? First of all there is the simple fact that, as said, we can observe a lot of synonymous variation in perfectly functional proteins. Of course we know that some synonymous mutations can affect function, mainly through alterations of splicing, translation and folding. There is great interest in that, especially for human diseases. However, the fact remains that most known genetic diseases are associated to non synonymous mutations. You can find a recent review about that here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4253807/ I quote a pertinent part:
Most tools focus on coding SNVs rather than other SNVs Decoding the relationship between genotype and phenotype is a major challenge in genetics. In humans there are more than four million DNA differences between two random individuals.22,23 Because additions and deletions typically have stronger impact,24–26 and are selected against more often, ?80% of these differences are single nucleotide variations (SNVs).27–29 Over the entire human population, an estimated 81%30 to 93%31 of human genes contain at least one SNV. Although only a small fraction of variants are non-synonymous single nucleotide variations (nsSNVs), about 10,000 are found between two random individuals,27–29 and over 85% of known disease associations are culled from this important class of mutations.1 For this reason, methods for predicting the impact of SNVs have historically focused on the high-yield category of non-synonymous coding SNVs. The existence of disease-associated synonymous mutations32,33 and nocoding variations with effects on lincRNA,34 miRNA,35,36 and promoters37,38 has produced interest in other types of mutations as well, but different tools will be needed to analyze these types of variations and such tools are comparatively still new and untested.39–41
Some synonymous mutations could act as weak deleterious events, for example as predispositions to diseases. In that sense, they could be considered "quasi-neutral". "3)you said: “Mutations are usually either neutral or deleterious.”- i think that most of them are actually deleterious. i show how in the fly example. if most of them was neutral then the fly genome need to be a lot more different then it is compare with the mosquito." I agree. But there is a lot of difference in those genomes, anyway. Probably neutral, but certainly also functional and designed. Otherwise, why would a mosquito be different from a fly? For example, I have blasted p53, an important transcription factor 385 AAs long in the fly, fly vs mosquito: there is only 35% identities and 52% positives in the AA sequence. That means that half the AAs are radically different. And yet both proteins are perfectly functional. And this is only the non synonymous variation. If we look at the synonymous variation, it will certainly be even greater, as expected for a protein which, however, is rather conserved (I have not done it because the process is longer, but if you want I can do it). More in next post.gpuccio
May 16, 2016
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Gpuccio: For me CD means only that engineering happens in existing living beings, and that what is not re-engineered is transmitted from one species to another.
Thank you for clarifying. Do you hold that — with the exception of the first organism — all species/information/sequences are introduced by CD? Are e.g. the Cambrian animals introduced by CD?Origenes
May 16, 2016
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Eric Anderson @119 Yes, you explained it very clearly. Thank you. Many biology research experiments must be done in vivo within real conditions through long time periods in order to reproduce valid situations, though that still doesn't guarantee recreating all possible scenarios. Since so much data obtained from wet labs is available in the cloud, dry labs can process it using valid algorithms. Work in progress... stay tuned. :)Dionisio
May 15, 2016
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Davem @112:
Most of us would agree that it’s impossible, yet we are to believe that somehow nature did it on it’s own?
Of course. You just have to believe real hard. And don't ask too many hard questions. :)Eric Anderson
May 15, 2016
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Dionosio @107: You touch on a very important point, and one that is very relevant to knock-out experiments and other claims of non-function. It is possible to have many, many things that are functional, but would not be observed as functional in particular circumstances or over particular timeframes. Redundancies, correction mechanisms, functions not required in a particular environment, built-in workarounds that mask the effect of the lost function, functions that are available but not activated (the front-loading idea), and so on. Then we have the whole suite of nice-to-have-but not necessary-for-immediate-survival functions, as you highlight. Until we know what is actually going on in organisms -- at an engineering level -- any claim that X is non-functional rests on shaky ground. The history of evolutionary claims about non-functional organs, vestigal features, and so on, enjoys the very dubious distinction of being nearly always wrong in the long term. We might do well to adopt a stance of caution about similar claims of non-function as we delve into the molecular realm.Eric Anderson
May 15, 2016
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Mung @92:
Perhaps we should cease to speak of common descent and speak of descent with modification. That might help distinguish the arguments, whether they are against shared descent or whether they are concerned with the means of modification.
Indeed, this is much of the disconnect -- at least among design proponents. Among traditional evolutionary theorists the two words "common descent" very clearly mean "purely natural, unguided, undirected, purposeless, common descent." I take it gpuccio, and if I understand him correctly, VJT (and Behe, for that matter), are talking about "descent with designed modification". Other than Biblical literalists, probably most design proponents could get behind that at some level -- or at least would be willing to consider it as a reasonable possibility. ----- Edit: I see that gpuccio @102 and bill cole @103 beat me to it. Keen minds running in the same vein and all that . . . :)Eric Anderson
May 15, 2016
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gpuccio @78: Thank you for the additional thoughts and for a view of where you are going. Just as an aside regarding whether the new discovers you point to regarding gene formation will have any impact on Darwinian claims, the answer, unfortunately, is no. You note that the options are:
1) Design or 2) RV + sheer luck (Remember, NS cannot be invoked here).
Quite true. Yet that has always been the case with almost everything Darwinian evolution claims to have produced. Behe's whole point with irreducible complexity, after all, was to highlight the folly of relying on natural selection for incomplete and inchoate phenotypic features. But the Darwinists muddle on, and, in those rare instances in which they are not shooting the messenger they invoke all manner of absurd explanations: co-option, HGT, neutral mutations that later inexplicably poof into beneficial mutations, and so on. Each of these proposed "mechanisms" is just another form of blind, dumb luck. There are myriad molecular machines in biology that don't have a chance of working without all their parts in place -- up front, coordinated, and controlled. And, by definition, everything has to be in place and built and functioning before natural selection can even waive its magic and mythical wand over the scene. Yet none of these engineering and logical constraints slow the Darwinist imagination one whit. Chance did it. Luck rules the day. Stuff Happens.Eric Anderson
May 15, 2016
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VJT: There have been a lot of comments since you responded, so I apologize if I'm missing an answer already given, as I'm just responding in order. You said:
The 340 beneficial mutations that are believed to have taken place in the human line during the same period represent only a tiny fraction (0.001%) of the mutations that were fixed in the human line, but it is these mutations that explain the important physical differences between humans and chimps.
Color me skeptical, but I am extremely skeptical of the proposition that 340 mutations turned an ape-like creature into a human. It just doesn't pass a basic credibility test. The simple fact is that we have almost no hard evidence about what changes would be required to turn organism A into organism B. We simply don't understand the engineering involved. But we do have some sense of the scale of the problem to build even one molecular machine. We also know that lots of information is involved in building an organism in addition to the raw DNA sequence. What we do know is that it is a massive engineering undertaking. What we further know is that at nearly every step of the way in this journey of discovery over the past 60 years the biological community has seriously and grossly underestimated the integrated, functional, information-rich complexity that is required to build even those machines that initially appeared to be simple. Until there is some real evidence -- I'm talking molecular-engineering-based evidence, not scratch-the-surface-database-comparisons of selected aspects of some portions of DNA -- until there is some real engineering understanding, any claim about what turned an ape-like creature into a human is little more than unsubstantiated speculation.
As I envisage it, many (but not all) of these mutations would have been intelligently directed.
Fair enough and reasonable enough. As a corollary, does that also suggest that we would not have expected 340 beneficial mutations within that timeframe, based on normal mutation rates?Eric Anderson
May 15, 2016
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Hi gpuccio, You asked me about the ratio of neutral to beneficial mutations: "After all, those numbers are derived assuming that no design intervenes. If you consider design as a true factor, then everything changes." I may be wrong, but as far as I can tell, the calculation for the number of neutral mutations in the human line makes no assumptions regarding design. The number is calculated using the postulates of the neutral theory. If you can show me where the calculations assume no design, then of course, I'm open to changing my mind.vjtorley
May 15, 2016
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Readers may wish to peruse the following articles, written in response to my post and to Professor Swamidass's article, "Evidence and Evolution": A Response to VJTorley by Dr. Cornelius Hunter. One Long Argument -- Responding to VJ Torley on Human-Ape Common Descent by Dr. Cornelius Hunter. Of Tree Rings and Humans by David Klinghoffer. Debating Common Ancestry by John West. Professor Swamidass has also written a follow-up article: Call for Response to the Tree I also wrote a short comment in response to Professor Swamidass's article, "Evidence for Evolution", which has been updated with an FAQ section:
Hi Dr. Swamidass, Thank you very much for your kind remarks about my post on Uncommon Descent. I’d just like to comment briefly on what you said about Dr. Hunter in the FAQ: “Third, I do believe that Dr. Hunter is not being intentionally deceptive or manipulative. I believe he is making a good faith effort, to the best of his abilities, to engage the evidence I have raised.” I would like to endorse what you said. I pulled no punches in my post, and on a few occasions, I did criticize Dr. Hunter for relying on flawed arguments. I also wrote that he “neglects to inform” his readers on a couple of basic points. For the record, I wish to make it quite clear that I am not accusing Dr. Hunter of being intentionally deceptive. All of us are, at times, guilty of an unintentional bias towards arguments that we personally favor, and it is all too easy to ignore what we might perceive as very minor or trivial problems in these arguments, when presenting them to an audience. That was what I had in mind when I wrote about Dr. Hunter’s “neglect.” Despite my differences with Dr. Hunter, I have the greatest respect for him as a Christian, and I would like to thank him for his forbearance and courtesy.
Cheers.vjtorley
May 15, 2016
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This is published in a Christian science venue hence his reference to what God has ordained. I assume Wilcox’s analysis is fairly accurate and if so what led to these differences between humans and chimps?
This was written poorly as I was between other projects. It should be a Christian venue on science. It is ASA. Definitely not Christian Science.jerry
May 15, 2016
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Try taking any kind of ape or monkey you want, and through selective breeding, create something similar to a human being. Most of us would agree that it's impossible, yet we are to believe that somehow nature did it on it's own?Davem
May 15, 2016
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From what I understand the difference between chimps and humans are not so much in the genome but in control sequences in the genome and in epigenetics and their effect of what proteins get expressed. http://bit.ly/1TfR5Ha
Despite our close genetic match with the chimpanzee, the human genome is radically different in its expression and radically different in its outcome. Though we share 98.7% of the same protein-coding sequences, the difference between our species is not in the 1.5% of the genome that codes for proteins, but rather in the 98.5% that controls their production. No other lineage has evolved as fast as ours, at least within the last 1.5 million years. The changes which differentiate us are primarily due to rapid changes in genetic control sequences. These changes involve every known class of control element, with the most profound changes found in the noncoding control elements shaping our neural system, especially the frontal cortex of the cerebrum. Further, the speed of the change is in large part due to the unique action of retrotransposons acting as “genetic engineers,” providing the raw genetic material selected in support of our cultural explosion. Although these are “natural” forces which we in part can understand, as Christians we should remember that they reveal what God ordained in eternity and realized through providence.
This is published in a Christian science venue hence his reference to what God has ordained. I assume Wilcox's analysis is fairly accurate and if so what led to these differences between humans and chimps?jerry
May 15, 2016
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about point 1)if the protein sequence havent realy changed (in the dna level)during one bilion years, then we can conclude that most of the mutations in this gene arent neutral. even for synonimous codons. do you agree with this conclusion? 2)do you have a reference that those exmaples are rare and not common? 3)you said: "Mutations are usually either neutral or deleterious."- i think that most of them are actually deleterious. i show how in the fly example. if most of them was neutral then the fly genome need to be a lot more different then it is compare with the mosquito. 4)you said: "Ka/Ks is a measure that is done on existing protein coding genes, comparing their nucleotide sequence."- can you explain how? thanks. as for 5) after another thinking i think its not a good example. so lets focus in the other point above.mk
May 15, 2016
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mk: I am not sure I understand all your points. Briefly: 1) I have read that post by Cornelius Hunter. In this particular case, I really disagree with his conclusions. As said, if you are interested we can discuss the issue in more detail. 2) No. The cases where synonymous mutations have detectable effects are rare, and the effect can be explained because of alterations in the translation rate. There is really no doubt that most synonymous mutations are neutral. They are so common: if they were not neutral, nothing could work in the protein world. They are common exactly for that reason: they are invisible to negative selection. 3) It's not that most of the mutations are functional. It is true that probably most of the genome is functional. Mutations are usually either neutral or deleterious. We know that well, even form human data. As I have tried to explain, neutral mutations are perfectly possible in functional DNA, because most of functional DNA has some tolerance to sequence variation, which is different from gene to gene. 4) You ask: "again- how its a fact if we assume that the sequence have been changed during million of years?" I don't understand what you mean. Ka/Ks is a measure that is done on existing protein coding genes, comparing their nucleotide sequence. It is an objective result, and as such it can be observed, The general pattern of those measures in the existing proteome is, again, an observable fact. There is no assumption here: you take the sequences, input them in your statistical software, and you get the numbers. What is your problem? You can debate the meaning of that pattern, not the pattern itself. If you have reasonable arguments about how to explain the pattern differently, I am here to listen. 5) You say: "its very important because its mean that many genes contradict the ka\ks ratio. if its was true that most of the bases are neutral then we predict that all the chimp genes need to be closer to human then gorilla. because they represent the time they split off (aka neutral clock)." I have never said that most of the changes between chimp and humans, or gorilla and humans if you prefer, are neutral. Indeed, if you read my post #86, you can see that I argued with VJ, saying clearly that IMO many of those changes can be designed, and can affect regulatory procedures. The Ka/Ks ratio can be computed only in protein coding genes. Protein sequences are very similar in primates. In short evolutionary times (a few million years) even synonymous mutations are rare. I have not computed any Ka/Ks ratio between chimps, gorillas and humans. Have you any data about that which contradict the meaning of the ration itself? Can you give the references?gpuccio
May 15, 2016
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1)first about the histone protein. dr hunter post about this here: http://darwins-god.blogspot.co.il/2012/12/how-evolutionists-stole-histones.html and if its true then why its so conserve? 2)if we found that even synonimous mutations can effect the protein function- then the whole Ka/Ks ratio is in doubt. 3)if most of the mutations are functional (like in my fly example)- then we cant consider those as neutral. 4)you said: "We have a definite pattern of Ka, Ks and Ka/Ks ratio. That is an observable fact" again- how its a fact if we assume that the sequence have been changed during milion of years? 5)you said: "I have no special idea about the relationship between gorilla and humans as compared to chimp and humans. I don’t even consider it a very important issue, and it is certainly an issue about which I know very little."- its very important because its mean that many genes contradict the ka\ks ratio. if its was true that most of the bases are neutral then we predict that all the chimp genes need to be closer to human then gorila. because they represent the time they split off (aka neutral clock).mk
May 15, 2016
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gpuccio @100
True functionality is proven in the wild, and in long times.
Yes, for example, as I've mentioned this before, if they'd get rid of all the small TV screens attached to the back of the seats in economy class in some airliners long routes, the airplanes will still fly well. Hence, one could safely conclude that those TV screens are completely unnecessary to fly the airplanes. But do they make a difference in the airliner's business regarding the services and conveniences they offer compared to their competition? Those TV screens have no functionality as far as the airplanes' flying mechanisms are concerned, but they make a difference in the airliner's business. However, how can we test that? Definitely not by just flying the airplanes. Maybe they would need to see how business goes during some time after the removal of that stuff from the cabin seats? Hence the test would have to be done in the real environment and for some time. Maybe then the experts could see if the removed artifacts were functional or not for the passenger's comfort and satisfaction, specially compared to the competition. Could we draw some analogies with the biological systems?Dionisio
May 15, 2016
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