The Revenge of the Guinea Pigs

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The nested hierarchy of DNA/Protein sequence similarity is powerful evidence for common descent. The parallel hierarchy formed by broken genes is more powerful still. Even anti-evolutionist Dr. Michael Behe accepts it as evidence of common descent. Behe’s acceptance of the evidence from broken genes confuses the conventional creationists, as seen in a report of a recent creationist forum. However, the creationists think they have a way out, but wouldn’t you know it, they are wrong.

Creatures inherit their DNA from their parents, who have inherited their DNA from their parents and so on into the past. We use this information to do paternity tests, and form genealogies. The nested hierarchy of DNA similarity is evidence that organisms descended from a common ancestor. Creationists try to deny this of course, and often invoke the idea that the similarity between organisms proteins reflects common design, that the proteins are similar because they have similar function. They never explain why, for example, the DNA sequences of the Tasmanian Tiger, a carnivorous marsupial that fills the niche of wolves (and looks pretty wolf-like), is much closer to that of the vegetarian Kangaroo than to the wolves, dogs and foxes whose ecological role and function they duplicate. Or why housekeeping genes with the same function, which are not dependent on the animals environment, also from this hierarchy.

Thylacine_Tree_2a.pngPhylogeny based on the sequence cytochrome b. The mid-sized carnivore the Tasmanian Tiger is shown to be more closely related to the vegetarian Kangaroo, and bandicoots and possums, than to its ecological niche and functional equivalents the dog/wolf family. As well, the sequence of the vegetarian Panda is more similar to carnivorous Bears than to other herbivorous animals

Despite the glaring flaws in the creationist “similar function” argument, it would good to have another line of evidence for ancestry. This evidence comes from broken genes (pseudogenes) in our genome. The genome is littered with non-functional sequences (indeed there are more non-functional sequences than functional genes), ranging from parasitic non-coding sequences like LINES to old broken viruses and broken genes. Over time, these sequences acquire mutations, organisms that share a recent common ancestor will have accumulated fewer mutations than organisms that have a distant common ancestor. These sequences also form a nested hierarchy that parallels the pattern we see with functional genes. It is very hard to argue that a nested hierarchy of broken genes represents common design (unless the Designer is the Sirius Cybernetics Corporation). The classical example of a broken gene in the human lineage is the gene L-gulono-gamma-lactone oxidase (GULO), which catalyses the last step of ascorbic acid biosynthesis. It is broken in primates, hence we get scurvy when we don’t eat fresh fruit or vegetables. Aligning the sequences of primate GULO genes shows humans being related to primates, with the chimpanzee being our closest relative.

As I mentioned, the nested hierarchy of the broken version of the GULO gene is powerful evidence of common ancestry. The Guinea Pig also has a broken GLUO gene, but it is broken in a different way to the primate genes, and does not nest with them. Dr. Michael Behe accepts data such as the nested hierarchy of the broken GULO genes as evidence of common descent. This confuses the creationists (isn’t Behe on our side?). At a recent creationist forum Paul Nelson tried to help a such a confused person by attempting to explain away the GULO evidence. However, his “explanation” was based on an error.

In 2003 the Nishikimi group compared the sequences of primate, Guinea Pig and rat GULO genes. The found that some sections of the Guinea Pig sequence matched the primate sequences more closely than rat sequences. They proposed that there were “mutational hotspots” in the GULO allowing convergent evolution between Guinea Pig and primate sequences. Some creationists immediately jumped on this paper, claiming that these alleged “mutational hotspots” invalidated common descent. This is a complete furphy. As mentioned above and as can be seen from the phylogenic tree below, the Guinea Pig nests more closely with rodents, and nowhere near the primates.

GULO_PHYLIP_Tree_Common_names.png Phylogenic tree of GULO sequences. As can be seen, the primate sequences nest together, with the chimpanzees and humans closest, as has been found with other genes. Guinea Pigs (Cavia) are closer to rodents (Mus; mouse and Rattus; Rat) than primates. Sequences aligned with MAFF and trees generated with PHYLIP.

One problem with the “mutational hotspot’ idea is that it is completely wrong. To claim that Guinea Pig and primate sequences have converged, you have to compare them with a sequence that is more representative of the ancestral sequence. Nishikimi’s group compared Guinea Pig and primate to rat sequences. However, it is the rat that has evolved significantly from the ancestral sequence, not the Guinea Pig and primate that have converged.

GULO_CLUSTAL_ALIGN_V2.jpg Alignment of mammalian GULO sequences (click to get larger version). The arrows indicate nucleotide positions where Nishikimi (2003) claimed that Guinea Pig and primate sequences had converged. As can be clearly seen, it is Guinea Pig (highlighted) and primate that retain the ancestral sequences, and the rat has diverged from this common sequence.

As can be clearly seen in the above diagram, the rat sequence has diverged from the ancestral sequences. So no mutational hotspots; Nishikimi was incorrect (and has admitted so in private correspondence). But that’s the good thing about science, it is self correcting, if we make mistakes, we fix them when new data comes out.

What gets me is that creationists could have done this analysis of GULO genes themselves (like the other analysis I have reported on). I used entirely public databases and web-based programs to do the trees and alignments. The Creationists did nothing, and are propagating an error.

228 Comments

Nitpick here … small typo in this sentence -

Dr. Michale Behe accepts data such as the GULO gene as evidence of common descent.

“creationists could have done this analysis of GULO genes themselves”

As if!

Fixed typo. Thanks!

Spotted another little typo, I think. :-)

As I mentioned, the nested hierarchy of the broken version of the GULO gene is powerful evidence of common ancestry. The Guinea Pig also has a broken GLUO gene, but it is broken in a different way to the primate genes, and does not nest with them.

As can be clearly seen in the above diagram, the rat sequence has diverged from the ancestral sequences. So no mutational hotspots; Nishikimi was incorrect (and has admitted so in private correspondence). But that’s the good thing about science, it is self correcting, if we make mistakes, we fix them when new data comes out.

Have there been published articles concluding that Nishikami was wrong ? My Pubmed search couldn’t seem to find any, or I may have been choosing my keywords wrong.

In the absence of the above, it would be helpful if Nishikami’s more recent views, expressed privately in his correspondence, could be given as much publicity as his original study.

So, once again, we must ask the IDiots to “Go stick your head in a pig” ;-P

CDV said:

Have there been published articles concluding that Nishikami was wrong ? My Pubmed search couldn’t seem to find any, or I may have been choosing my keywords wrong.

In the absence of the above, it would be helpful if Nishikami’s more recent views, expressed privately in his correspondence, could be given as much publicity as his original study.

No, there is currently no peer-reviewed paper, although it is pretty well understood by the phylogenetics community. I will see if I can get permission to quote Nishikami’s response. It is not clear if Nishikami is intending a follow-up paper or corrigendum.

Try for a moment to think like someone who truly has a problem with common descent. Specifically, that you seriously thought various groups of animals (all eukaryotes) originated independently from nonliving matter. The first thing that you’d want to do is avoid weasel words like “common design” because how better to implement “common design” than by descent with (possibly radical) modification? Second, you’d avoid reference to design altogether, because a designer could actuate that design anyway he wanted. Even Richard Sternberg admits that. Third, you’d avoid finding weakness with “RM + NS” because, as Behe will tell you, that does not refute common descent. Fourth, you would avoid at all costs “improbability of abiogenesis” calculations, because your “theory” requires many abiogenesis events (of eukaryotes, no less), whereas common descent can accommodate a single, extremely rare event.

If your objection is only about common descent, you might also want to make it perfectly clear that you have no objection to the chronology of biological history that is agreed upon by many fields in science, not just evolution. And to further dispel any doubt that you are serious, you’d be very clear about when those new lineages arose from nonliving matter. Even if they were just tentative “best guesses,” you’d assure us that you planned to test them, and reject them if necessary.

Lets also say that, like creationists and IDers, you don’t conduct original research, but just sit on the sidelines and evaluate work done by others. What then would be your argument against common descent? Simple, you would analyse the hypotheses and conclusions of people like Schwabe, Senapathy and Goldschmidt, and argue why Goldschmidt is the odd man out. To further assure that your objection is strictly scientific, you’d challenge Behe directly - again with no reference to his design argument. And you’d never have to use the word “Darwinism.”

Note, by “animals (all eukaryotes)” I mean “animals (all of which are eukaryotes),” not necessarily that you thought that every species of eukaryote originated independently.

You people really should ignore the YEC crowd, the creos arguing against common descent. It just mucks things up. I always ignore their nonsense; and I don’t have near the contempt for them that most neo-Darwinan atheists, and the occasional neo-Darwinian theist, have. Hell, some of my best friends are YECs. Just refer them to Behe, and forgetaboutit. If Behe can’t convince them, trust me, you neo-Darwinian atheists never will.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

Again, if you want to show that evolutionary processes, and ID focuses almost exclusively on Darwinian processes, are insufficient then you have a long road ahead of you since, contrary to Behe’s ‘argument’ based on an off-hand guestimate, evolutionary processes are shown to be much more clever than the ID Creationists who deny their capabilities. Of course, also realize that ID conflates our ignorance with evidence in favor of design and ID, that is what makes ID so meaningless. Not to mention that ID has yet to contribute anything non-trivial to scientific understanding.

If you are betting on Behe then you have lost already.

The only actual issue is how much evolution can actually be shown (preferably quantitatively rather than through just so stories) to have resulted from RM+NS. To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

Again, if you want to show that evolutionary processes, and ID focuses almost exclusively on Darwinian processes, are insufficient then you have a long road ahead of you since, contrary to Behe’s ‘argument’ based on an off-hand guestimate, evolutionary processes are shown to be much more clever than the ID Creationists who deny their capabilities. Of course, also realize that ID conflates our ignorance with evidence in favor of design and ID, that is what makes ID so meaningless. Not to mention that ID has yet to contribute anything non-trivial to scientific understanding.

If you are betting on Behe then you have lost already.

Tell us, bigbangBigot, why are gain-of-function mutations, both single and series of, considered “degradation”?

bigbang said:

To those of us that don’t blindly accept the neo-Darwinan/Dawkins party line, most would bet our left testicle that beyond simple mutations that are almost always a degradation of sorts—-and that result in things like microorganism drug resistance, human resistance to malaria,” Antarctic icefish “antifreeze” (and also the development of that HIV viral protein-vial protein binding site that Behe unfortunately overlooked when writing EoE, but has now acknowledged as having evolved apparently after RM+NS had around 10^20 shots at it, numbers similar to malaria’s CQ resistance), etc.—-not much.

Betting parts of your anatomy when there is evidence out there is a foolish business. The idea that mutations always represent degeneration is a YEC notion that has been long shown to be wrong (for example: the ability of bacteria to breakdown nylon, pentacholophenyl and atrazine are due to the development of new enzymes).

As well, there is a lot Behe gets wrong. The HIV Vpu ion channel evolved after much less than 1020 “shots” as you call them, see my open letter part 6 where I discuss how Behe has gone badly wrong in detail.

bigbang,

Arguing that evolution is theoretically impossible is futile. This evidence shows that it in fact did occur. What is your explanation for the nested hierarchy of genetic similarities shown in the phylogeny? Remember that this was drawn using pseudogene sequences. How do you account for the fact that this phylogeny is congruent with the relationships shown by every other data set? Why do you think that hand-waving arguments are more convincing that actual evidence?

that beyond simple mutations that are almost always a degradation of sorts—-

That is false and this has been known for a century.

Within recent human evolution alone, we have examples of the selective sweep of duplicated amylase genes, adult lactose tolerance, and a new mutation that confers resistance to artherosclerosis, A1 Milano. None of these are loss of function mutations. One is a gene duplication.

Waving your hands and repeating lies and fallacies doesn’t prove that evolution is impossible. It proves you have too much time on your hands and you lost your library card.

Beneficial mutations are common in any system one cares to look at.

Speaking of phylogeny, I was intrigued by press release on a possible new method to sort out ecological niches among bacteria. Apparently it is a hard problem.

The solution? Perhaps to sequence them wholesale and identify niches by phylogeny:

Microbes drive almost all chemical reactions in the ocean; it’s important to identify the specific professions held by different groups.

Polz and former graduate student Dana Hunt, now a postdoctoral researcher at the University of Hawaii, created a large and accurate genetic data set by isolating and identifying over 1,000 strains of vibrio bacteria from a sample of eight liters of seawater gathered near Plum Island, Mass., in the spring and fall.

“What is really new about our approach is that we were able to combine both molecular data (DNA sequences) with ecological data in a single mathematical framework,” said Alm. “This allowed us to solve the inverse problem of taking samples of organisms from different environments and figuring out their underlying habitats. In essence, we modeled the evolution of a microbe’s lifestyle over millions of years.”

So to get a grip on ocean chemistry of today, we may have to take the shortcut of sorting out bacterial evolution over millions of years. Also the authors argue that these populations are efficiently separated, so they would constitute the equivalent of species in spite of being (poorly) resolved but closely classified by taxonomy.

ID creationists can’t resolve such results if they stand up, for them evolution can’t be important, and bacterial adaptation is only “evolution in the small”.

PS. 1h30’ until Phoenix touchdown. As we all know Phoenix is going after the water and its chemical environment, both for manned trips but also for astrobiology. Another bummer for creationists.

Also the authors argue that these populations are efficiently separated,

Correction, this is what they seem to argue to me.

Quoting from the head of the page: “Creatures inherit their DNA from their parents, who have inherited their DNA from their parents and so on into the past. We use this information to do paternity tests, and form genealogies. The nested hierarchy of DNA similarity is evidence that organisms descended from a common ancestor.”

As a juvenile sitting in a classroom can see, the first sentence in that quote absolutely rules the final sentence out of all realms of possibility. Or is someone going to explain why common descent doesn’t equal “creatures inherit[ing] their DNA from their parents”, said DNA enabling scientists “to do paternity tests”?

By definition of the “common descent” being called upon, the best that DNA might be able to do is enable scientists to attempt nested hierarchy membership tests, no certainty issuing therefrom. Your particular DNA might show you are a throwback to a wobbygong. But there is a rational alternative to this business of publicly walking about on the ceiling.

bigbang Wrote:

You people really should ignore the YEC crowd, the creos arguing against common descent. It just mucks things up. I always ignore their nonsense; and I don’t have near the contempt for them that most neo-Darwinan atheists, and the occasional neo-Darwinian theist, have. Hell, some of my best friends are YECs. Just refer them to Behe, and forgetaboutit. If Behe can’t convince them, trust me, you neo-Darwinian atheists never will.

I don’t have any contempt for rank and file creationists, YEC or OEC. If anything I want to help them from being scammed by the “don’t ask, don’t tell” gang. You might notice that I rarely miss an opportunity to refer them to Behe. But thanks for making it clear that your objection to evolution has nothing to do with the science, and all about the atheists and occasional theist.

If you don’t find arguments against the antiquity of life or common descent convincing, then the last thing you want to do is sweep them under the rug. Many YECs and OECs do change their mind when shown how they have been misled. Some, like Glenn Morton feel obligated to educate others about it.

PBH,

What is your explanation for the nested hierarchy of genetic similarities displayed in the phylogeny? Why does this data reveal exactly the same pattern as displayed in other data sets?

The Phoenix lander has successfully touched down on Mars. http://www.nasa.gov/multimedia/nasatv/index.html

The lander carries a CD which includes the names of my children.

No images yet, but the lander is sending back telemetry and has landed somewhere flat “like a table” someone just yelled. Soon it will begin it’s search for water.

D.S.,

Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion.

When speciation occurred - it was instantaneous in terms of geologic time - DNA was adjusted/re-programmed, the species lock was tripped and a new lock was set, a new species immune system likewise had to be set, and so on. These are all things that are theoretically possible. Speciation itself presumably implicated genetic engineering and something approximating to surrogate motherhood, done via quantum category info. technology, operating in Nature. Again, theoretically possible.

The re-programming of the genetics (with total species information, in one hit) implicates more than one source of empowering and information input: the empowering signalling had something to do with celestial bodies, especially the sun-earth-moon system; but the observed modification in keeping with environmental requirements suggests information storage and retrieval in the information bank of the organism itself. On top of this we have the observed fact that planning capacity in the form of genes is passed on from species to species, which said capacity was activated by the onset of relevant environmental conditions.

So we have information capacity, we have information signalling, we have mechanisms that respond to readable signals, we have an increasing spread of genetic capability as evolution proceeds. Information, playing on a finite array of “keys”, to produce music. Each species unique, because of the abundant permutations and combinations available. Each species suited in some ways to environment, because the inbuilt information reading/response capacity promotes it. All species having commonality of genetics, because they were evolved under the same info. tech. system which accessed the collection of genetic options available.

Conduits, not blood ancestors. Common Descent evolution is about equivalent to charting the North-West Passage in a timber ship, with lead food tins for the crew.

Given that the Earth coalesced in or with the assistance of something like water, probably H2O, itself, there is no reason why other planets might not have done the same.

Congratulations on this achievement. Can we hear the CD?

Philip Bruce Heywood said: Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion.

I call Poe’s Law on PBH!

Philip Bruce Heywood said:

D.S.,

Species were conduits of life, not blood ancestors. There is a total difference, but nevertheless it is easy to confuse the conduit notion with the ancestor notion.

When speciation occurred - it was instantaneous in terms of geologic time - DNA was adjusted/re-programmed, the species lock was tripped and a new lock was set, a new species immune system likewise had to be set, and so on. These are all things that are theoretically possible. Speciation itself presumably implicated genetic engineering and something approximating to surrogate motherhood, done via quantum category info. technology, operating in Nature. Again, theoretically possible.

The re-programming of the genetics (with total species information, in one hit) implicates more than one source of empowering and information input: the empowering signalling had something to do with celestial bodies, especially the sun-earth-moon system; but the observed modification in keeping with environmental requirements suggests information storage and retrieval in the information bank of the organism itself. On top of this we have the observed fact that planning capacity in the form of genes is passed on from species to species, which said capacity was activated by the onset of relevant environmental conditions.

So we have information capacity, we have information signalling, we have mechanisms that respond to readable signals, we have an increasing spread of genetic capability as evolution proceeds. Information, playing on a finite array of “keys”, to produce music. Each species unique, because of the abundant permutations and combinations available. Each species suited in some ways to environment, because the inbuilt information reading/response capacity promotes it. All species having commonality of genetics, because they were evolved under the same info. tech. system which accessed the collection of genetic options available.

Conduits, not blood ancestors. Common Descent evolution is about equivalent to charting the North-West Passage in a timber ship, with lead food tins for the crew.

Got a little problem there, Haywood.

No evidence to support you. Kinda of a stopper, don’t ya think?

Folks, don’t feed trolls. And don’t quote large amounts of other peoples text, it makes following the thread hard. Thanks for your consideration.

Philip Bruce Heywood said:

Quoting from the head of the page: “Creatures inherit their DNA from their parents, who have inherited their DNA from their parents and so on into the past. We use this information to do paternity tests, and form genealogies. The nested hierarchy of DNA similarity is evidence that organisms descended from a common ancestor.”

As a juvenile sitting in a classroom can see, the first sentence in that quote absolutely rules the final sentence out of all realms of possibility. Or is someone going to explain why common descent doesn’t equal “creatures inherit[ing] their DNA from their parents”, said DNA enabling scientists “to do paternity tests”?

Mutation, PBH, mutation. All it takes is an occasional mutation that is passed on to the next generation.

Scott said:

I call Poe’s Law on PBH!

No. Although he lies about other things I think he genuinely believes this. Visit his website for an eye-opener.

So then PBH, you have absolutely no explanation why the pattern observed in pseudogenes should correspond precisely to what is expected if common ancestry is true. Your incoherent mumblings do not even begin to address the issue and from what I can tell, your supposed hypothesis is completely inconsistent with the observed pattern. Why in the world would some “info tech system” produce the exact pattern expected from common ancestry in nonfunctional genes? Once again, all you have is wishful thinking.

Behe, a Catholic and microbiologist

And once again, someone looks at Behe’s scientific qualifications, and finds his religion not only relevant but primary. THEN we have his background. THEN we have…uh, check that, the evidence doesn’t actually make the list. It’s not Behe’s utter lack of evidence, research, or even hypothesis that disturbs us, it’s Behe’s religious faith! What else COULD it be, in the eyes of someone armed with faith but no evidence? Behe’s “insight” consists of avoiding evidence at all costs.

Dang, forgot to mention that Behe used to be a biochemist, NOT a microbiologist. He only plays one when he’s not on witness stands.

Flint sez…

This may or may not be a semantic quibble, but I’ve yet to see any good indication that creationists really understand what evidence means.

The closest I’ve seen any of them come is, speculations … that support their foregone conclusions are “evidence”.

I agree wholeheartedly. Too many times I’ve heard the standard “well, you choose what you call your evidence and I’ll choose mine” argument used by the creobots who want to use the Bible of proof of creation equaling the evidentiary value of boxes of fossils and databases of DNA.

They cannot fathom that “evidence” has some deeper meaning than “That which frames my argument”.

These are the same shining intellectual lights that tell their kids to interrupt biology classes with “Were you there?” because in their book, that’s a compelling argument. (As an aside, did you ever notice how they never seem to want to answer “Were you there when the Bible was written?”)

PvM said:

Genetic degeneracy… Small difference but big in its extent. In fact, natural selection is part of the explanations for the origin and evolution of the genetic code. In fact, the degeneracy of the genetic code may not just be an important reason for the success of evolutionary processes (evolvability) but it should also be realized that such neutrality can in fact be under selective pressures.

Just because the genetic code evolved in manners that involved other processes than just natural selection does not mean that NS was falsified, on the contrary.

peter borger, biologist, PhD said:

“Some theories such as natural selection are so well validated that it is hard to falsify them these days. Which is what the National Academy of Sciences said in their recent statement on evolution.”

Apparently they never heard about genetic redundancy.

Apparently, you also are unaware of genetic redundancy and how it is defined. I was not talking about the genetic code. I was talking about “the situation in which a gene is selectively neutral”. In spite of the beautiful not-falsifiable algebraic formulation of natural selction, we still have the no-phenotype knockouts. No phenotype double knockouts, triple, etc. Kilobases of conserved DNA can be knocked out in mice with no effect on fitness and reproduction. That tells me NS is irrelevant explaining the genomic content. I thought I was clear about that. Furthermore, Truman and I wrote a series of articles about the genetic code and why it couldn’t have evolved by NS. BTW, there is no degenracy in the code. There is redundancy. It appears to be the best code possible to buffer errors. It most have been there from the start. And it tells me it is a product of ID. NS = phlogiston.

Ian, why are you unable to discuss the topic without being condescending? Is it so hard to keep up the paradigm?

I used to work in the hematology lab where most of my colleagus studied AMLs. The finding was that translocations were in 80% on exactly the same spot. I’ve seen the data, they’ve been published and it made me think about the true nature of how mutations might be introduced: non-stochastic. That is about 13 years ago, when I still was a PhD student. I have had a long way to think about the matter. When everybody was setting up new ad hoc hypothesis to explain away the data that falsify Darwin, my midn already wopkde on a novel theory. Now, a decade later I know how to determine what part of mutaions is non-random. I know several mechanism that give an illusion of common descnet. I will present them in my forthcoming book. That will be the end of the Darwinian era.

How do we discriminate between a super hot spot that changed in the past in several species independently and a position you take as evidence for common descent? Position 97 might be such position. Because of HAR1F and other Darwin CD falsifying observations I take it as a NRM; A super hotspot that fixed independently in primates because of a severe bottleneck.

Ian, Regarding the Drosophila paper (I thought you said I had to stay on topic: GULO).

Anyway,

In this paper, Karl J. Schmid and Diethard Tautz, two biologists of the University of Cologne discussed fast evolving genes in Drosophila melanogaster and Drosophila simulans. The focus was on the 1G5 gene. This gene is found in both species as a unique single copy gene; it is of unknown function but not an inactive pseudogene. The 1G5 gene had the authors’ particular interest because it was the fastest changing gene of their study. From protein coding part of the 1G5 gene counts 1’081 base pairs, which includes only one small intron of 61 base pairs. Schmid and Tautz located all mutations in an 864 base pair segment, which included the intron, in thirteen populations of D. melanogaster and four of D. simulans. It turned out that the major part of the individual genes is identical and not interesting for analysis. Only a handful of mutations was observed between the subpopulations of fruit flies a few dozens between the two species. Most of them are point mutations, but there are also indel mutations of more than one nucleotide in this part of the gene. The left side of figure 16-1 shows the mutations observed in the 61 base pair intron; the right hand side shows the mutations in the 803 base pair fragment of the coding region (exon 2). The numbers 141 to 922 at the top of the figure indicate the exact location of the mutations present in the 1G5 gene. It shows that the fraction of variable sites in the non-coding part (the intron) and the protein-coding part (the exon) of the 1G5 gene is approximately the same. The authors concluded that:

Almost none of the amino acid positions may be under strong selective constraint, because the fraction of polymorphic sites in the intron is comparable to the fraction of polymorphic sites in the coding region. […] Comparison between fixed and polymorphic sites between the two species shows also no significant deviation from the assumption of a neutral evolution in this region.

Is that all – neutral evolution in this region? Is there nothing more to say about the 1G5 genes? As a matter of fact the genes demonstrate some very intriguing phenomena that went unnoticed by the authors.

Let’s have a look at the figure they present (you have the article in front of you so look at it carfully).

The introns of the individual genes vary considerably between the two distinct species (13 out of 61 nucleotides are different: 21%), introns within subpopulations of D. melanogaster show nearly no variation (1 out of 61 nucleotides vary in only 3 out of 13 subpopulations: 1.6%). Similarly, introns in the 1G5 gene found in the subpopulations of D. simulans do not demonstrate variation at all. This is peculiar, since it is expected that the highest incidence of mutations is within the intron regions of a gene. The neutral theory tacitly assumes that introns are not subject to selection and accumulate mutations at random. This is not only expected in reproductively isolated species, but also between isolated subpopulations of one species. Yet, we do not see variation within the introns of subpopulations. A careful look at the positions of the mutations in the introns between the species shows the intron accumulated thirteen mutations of which ten are immediately adjacent to each other (numbers 153-162). The chance that ten point mutations occur at random in the intron equals 1.4 x 10-18. By way of contrast, the chance that ten adjacent mutations occur in the intron equals 2.2 x 10-14. Natural selection can’t explain this cluster of mutations. Introns are assumed to be evolutionary neutral, in that selection does not act on them. If you want to invoke Darwin’s magic word to explain the fixed cluster, it must have arisen by selection on neutral positions. That is neutral selection. It is therefore reasonable to assume that the cluster of mutations observed in the introns is not the result of chance.

Another remarkable observation is that the 1G5 genes in subpopulations of D. melanogaster, as far apart as Australia, Russia or Canada are completely identical. It implicates a very high level of stability of the DNA sequences within species. Even within the highly unstable 1G5 gene. Evolutionists may speculate that these identical populations were derived from a common founder population that repopulated the area after an ice age, or so. But, why would an Australian and not a Japanese or Mexican population of D. melanogaster - which would make much more sense - take over the empty niches in Russia and Canada? And even if it happened like that, it would not explain the observation of the invariable fixed intron in the 1G5 gene of D. simulans. Neither would it explain the cluster of 10 adjacent mutations in the introns of both species.

There is even more. A careful comparison of exon2 of the 1G5 gene of both Drosophila species uncovers that the genes change with distinctly different rates. Subpopulations of D. melanogaster demonstrate an average of nearly 3 mutations of 803 possible locations (0.37%), whereas subpopulations of D. simulans exhibit and average of 14 mutations (1.7%). Moreover, D. simulans, but not D. melanogaster, demonstrates insertion-deletion mutations in the 1G5 gene. Clearly, the genes change at different rates and suggest that the genes have distinct functions in either organism.

The sequences of the three Australian subspecies could’t descent from other without invoking NRM. Try it, and tell me how, if it is possible.

The data provided by Schmidt and Tautz showed that natural selection was unlikely to act on the 1G5 gene. The consequence is that the shared mutation in the 1G5 genes must be due to a biological or physical mechanism .

I discussed this years ago.

Scott Page commented then: A fluke.

Your comments now: migration.

What is it? NRM.

Ciao, Peter

Next, we can go through the ancient human mtDNA. I will again proof my point of NRM, Scott Page will jump in telling I am a moron, a fool, or whatever, and then in five years or so, I will do it again on another board.

History is repeating itself and nothing is going on in evoland.

Sleep well.

Peter

peter borger, biologist, PhD said:

In this paper, Karl J. Schmid and Diethard Tautz, two biologists of the University of Cologne discussed fast evolving genes in Drosophila melanogaster and Drosophila simulans.

I notice that you have not addressed my question. Where in the paper does it say that they sampled “endemic” populations?

Let’s have a look at the figure they present (you have the article in front of you so look at it carfully).

Oh, yes, lets do (and don’t forget, I’ve done my own alignments as well, with extra genes).

The introns of the individual genes vary considerably between the two distinct species (13 out of 61 nucleotides are different: 21%), introns within subpopulations of D. melanogaster show nearly no variation (1 out of 61 nucleotides vary in only 3 out of 13 subpopulations: 1.6%). Similarly, introns in the 1G5 gene found in the subpopulations of D. simulans do not demonstrate variation at all. This is peculiar, since it is expected that the highest incidence of mutations is within the intron regions of a gene.

If it is under nearly neutral selection, you would expect the variation rate within the exon to be pretty similar to that of the intron. And it is in D. melanogaster. There are only 3 D. simulans sequences in the paper, if the intron substitution rate in D. simulans sequences is roughly the same as D. melanogaster, then you would expect to see no variation with just 3 subtypes sampled. And indeed, if you sample more subspecies (there are now around 13 in the database), you see a polymorphism. It’s not a puzzle, just basic sampling statistics.

A careful look at the positions of the mutations in the introns between the species shows the intron accumulated thirteen mutations of which ten are immediately adjacent to each other (numbers 153-162).

Actually that’s an error. There is an indel, and the authors must have accidentally shifted the sequence over when making the table (or the software they were using stuck the indel in the wrong place as they were using so few D. simulans sequences, see how important it is to do your own alignments with up-to-date gene lists).

gaaattgtat ← melanogaster
–cctggcaa ← correct simulans, note no sequence of 10 differences any more.
cctggcaatg ← from table, wrongly aligned

If you had run your own alignments, you would have picked this up. There is no “run of 10” replacements. The rest of your analysis is meaningless.

Another remarkable observation is that the 1G5 genes in subpopulations of D. melanogaster, as far apart as Australia, Russia or Canada are completely identical. It implicates a very high level of stability of the DNA sequences within species. Even within the highly unstable 1G5 gene. Evolutionists may speculate that these identical populations were derived from a common founder population that repopulated the area after an ice age, or so. But, why would an Australian and not a Japanese or Mexican population of D. melanogaster - which would make much more sense - take over the empty niches in Russia and Canada? And even if it happened like that, it would not explain the observation of the invariable fixed intron in the 1G5 gene of D. simulans. Neither would it explain the cluster of 10 adjacent mutations in the introns of both species.

There were no populations of D. melanogaster in Canada (or the rest of the American continent) before around 130 years ago, and none in Australia before the 1900’s. All the D. melanogaster in the Americas and Australasian area are invaders. They mostly derive from Eurasian populations (which are pretty homogeneous), although there are a small proportion that derive from African populations.

An Australian population could not take over a Russian niche as there was no Australian population (or Japanese or Mexican population as there was no Drosophila in Japan before the 1960’s, and none in Mexico before around the 1900’s). Drosophila evolved in Africa, then invaded Eurasia. Humans then took Drosophila to the Americas and Australasia in their ships.

Eurasian and African Drosophila populations have entered the Americas and Australasia multiple times since the first colonization events. Here your analysis fails as you are ignorant of organsimal biology.

That backs up the HOX genes - paddlefish story and is as near to proof that anyone needs, that something far more sophisticated than mere NS was involved in evolution.

I fail to follow this reasoning. Imagine that a DNA test indicates that a child’s father is someone other than his mother’s husband. This happens from time to time. Does this constitute “as near to proof that anyone needs” that human breeding doesn’t work the way we think it does? That something “far more sophisticated” is involved?

What you’ve pointed out is a suggested change in the previously proposed clade diagram, which has nothing to do with the mechanisms by which clades evolve. So now a new diagram is proposed? OK, what’s the problem?

Ian Musgrave said:

There were no populations of D. melanogaster in Canada (or the rest of the American continent) before around 130 years ago, and none in Australia before the 1900’s. All the D. melanogaster in the Americas and Australasian area are invaders. They mostly derive from Eurasian populations (which are pretty homogeneous), although there are a small proportion that derive from African populations.

An Australian population could not take over a Russian niche as there was no Australian population (or Japanese or Mexican population as there was no Drosophila in Japan before the 1960’s, and none in Mexico before around the 1900’s). Drosophila evolved in Africa, then invaded Eurasia. Humans then took Drosophila to the Americas and Australasia in their ships.

The House Fly, Musca domestica also originates from Africa, had invaded Eurasia, and was transported to the rest of the world by humans.

Eurasian and African Drosophila populations have entered the Americas and Australasia multiple times since the first colonization events. Here your analysis fails as you are ignorant of organsimal biology.

The foundation of Creationism is always ignorance; some creationists make a bigger song and dance out of obfuscating this fact, but, it always comes back to haunt them as building upon ignorance is tantamount to building on quicksand.

PBH rants .…

Then there are ant-creationists who send articles out of NATURE, and SCIENCE, and such like, to the bathroom wall - ONLY IF THE ARTICLE DOESN’T SUIT THEIR POINT OF VIEW. Then they sit on the white throne of “science”, and say that everyone else is ignorant.

I call Shenanigans.

Bring forth the links to those comments on the wall, Phil, or shut forth the mouth.

(Sadly, I predict he will do neither).

Flint said:

That backs up the HOX genes - paddlefish story and is as near to proof that anyone needs, that something far more sophisticated than mere NS was involved in evolution.

I fail to follow this reasoning. Imagine that a DNA test indicates that a child’s father is someone other than his mother’s husband. This happens from time to time. Does this constitute “as near to proof that anyone needs” that human breeding doesn’t work the way we think it does? That something “far more sophisticated” is involved?

Well, that depends on if the parents are good god-fearing christians. Because everyone knows it’s impossible there could be any adultery in such a family. So if such a test result occurs among True Christians™, it must be proof of some heretofore unknown supernatural mechanism of birth, or proof DNA doesn’t exist, or proof the kid’s the Second Coming or some such. If the parents aren’t True Christians™, then it just means mom’s a slut. Even if they did in-vitro fertilization, or Dad’s had all his bone marrow replaced so the DNA in his blood doesn’t match anymore, it’s always best to use the most evidence-free, mysogynistic explanation to discredit anyone who isn’t a True Christian™. Facts have a well-known liberal bias.

Flint said:

What you’ve pointed out is a suggested change in the previously proposed clade diagram, which has nothing to do with the mechanisms by which clades evolve. So now a new diagram is proposed? OK, what’s the problem?

Let’s see, which response to a tiny change in the diagram would be most appealing to a creationist?

1. Modify the diagram in light of the new evidence.

2. Set the diagram on fire, give up on looking for rational explanations, bow down and praise Jeebus.

“The foundation of Creationism is always ignorance”

Was I talking about creationism? No, I was talking about Non-random mutations. Because you can’t show how the populations werde derived from each other in a diagram, it leaves us with the only option of non-random mutations in the 1G5 genes to explain the alignment of several mutations.

If not, show how they evolved. Scott page couldnt, I can’t, and you cannot.

We can’t, because the mutations are not introduced at random.

Goodbey, Darwinism.

Ian, continues his condescending style:

“The foundation of Creationism is always ignorance”

I wasn’t talking about creationism, I was talking about non-random mutations. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that?

Because you can’t show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations.

If not, show how they migrated and evolved.

If it can’t be done, the mutations are introduced in a non-random fashion.

Sorry, it wasn’t you comment. It was some other guy. My response should read:

peter borger, biologist, PhD said:

Ian,

I was talking about non-random mutations in D mel’s 1G5 gene. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that?

Because you can’t show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations.

If not, show how they migrated and evolved.

If it can’t be done, the mutations are introduced in a non-random fashion.

That’s all, and you are right about the populations being introduced recently.

The revenge of the Drosphila:

Ian says, and I agree:

“There were no populations of D. melanogaster in Canada (or the rest of the American continent) before around 130 years ago, and none in Australia before the 1900’s. All the D. melanogaster in the Americas and Australasian area are invaders. They mostly derive from Eurasian populations (which are pretty homogeneous), although there are a small proportion that derive from African populations. An Australian population could not take over a Russian niche as there was no Australian population (or Japanese or Mexican population as there was no Drosophila in Japan before the 1960’s, and none in Mexico before around the 1900’s). Drosophila evolved in Africa, then invaded Eurasia. Humans then took Drosophila to the Americas and Australasia in their ships. Eurasian and African Drosophila populations have entered the Americas and Australasia multiple times since the first colonization events.”

The sequences show:

An Italian population invaded the Americas, first the USA (D. mel III) and then it migrated to Peru. In Peru this population acquired the exact same mutation as, and independent of, the population in Japan (the A at position 835). A population of Cyprus, Irak or USSR invaded Canada and USA (USA II). The populations in Australia were not derived from the Italian. Still, the Australian population ends up with the exact same mutation the Italian population acquired in the USA (The C at position 498).

The Australian population (D. mel 3) could have migrated from the USA (D mel 11), and acquired an A at position 637.

Conclusion:

1) mutation rates are high,

2) mutations are not merely introduced at random.

peter borger, biologist, PhD said:

Ian,

I was talking about non-random mutations in D mel’s 1G5 gene. Whether or not the indel shifted or got lost is not relevant to observe the NRM in D. mel. I thought you were going to respond to that?

Your claim of “non-random” mutation relies on the unusual co-incidence of a run of ten consecutive mutations. The misplaced indel changes everything, and there is now just a short run of non-consecutive mutations totally consistent with random mutations.

Because you can’t show how the D. mel populations were derived from each other, the nmigration and evolution pattern, it leaves us with no other option of non-random mutations in the 1G5 genes in D. mel. to explain the alignment of several mutations.

If not, show how they migrated and evolved.

If it can’t be done, the mutations are introduced in a non-random fashion.

By the way, you still haven’t pointed out in the paper of Schmid and Tautz they say they used “endemic” populations. I wonder why that is? smiles sweetly

Oh, dear. You don’t have a diagram in front of you, so D. melanogaster must have been independently created in the US in the 1870’s, and in Australia in the 1900’s. It’s a miracle! (that was sarcasm by the way).

Well, I’m looking at a nice map of the arrival and spread of D. melanogaster in the US right now. How about you do some work for a change and loom up the history of D melanogasters spread. (hint: search Current Biology with drosophila and history in the search terms. Hard isn’t it. You might profitably look up the data on mtDNA heterogeneity and the spread of P elements in the 1950’s)

By the way, did you ever get around to running a phylogenetic tree on the GULO gene with the indel at position 97 replaced with G? No, I didn’t think so. Here’s the tree I generated (finally worked out how to do ASCII art in XHTML), and guess what? You still get a nice common descent tree. Indel at position 97 isn’t creating an illusion of common descent at all (you get the same sort of thing if you replace G with random bases, the bootstrap probability is lower, but you still recover the primate tree)

         +-------------Mustellus
     +--10  
  +--9   +----Platypus
  |  |  
  |  +Horse
  |  
  |  +----Guinea Pig
  |  |  
  |  |          +--Macca
  |  |     +----8  
  |  |     |    |  +Pongo
  |  |     |    +--7  
  |  |  +--5       |  +Human
  |  |  |  |       +--6  
  |  |  |  |          +Chimp
  1--2--4  |  
  |  |  |  +--Dog
  |  |  |  
  |  |  |  +-Rat
  |  |  +--3  
  |  |     +Mouse
  |  |  
  |  +Pig
  |  
  +--Cow

Look, Peter, boasting how you are so much better than us because you are a biologist while completely overlooking basic biology is not how a scientist works. Sitting on your bottom and demanding we run around and find data you should have been aware of in the first place is not how a scientist works. Sticking your fingers in your ears and singing “la la la I can’t hear you” when presented with data that shoots down your ideas isn’t how a scientist behaves.

If you want to be respected as a scientist, act like a scientist.

Not that this comment thread hasn’t been fun, but I have to prepare for the Australian Society Medical Research congress and read my students final PhD Thesis draft. As I won’t be able to monitor the thread, and to stop trolls taking over, I’m going to turn off comments.

People who wnat to follow up Trolls on the bathroom wall, go here

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This page contains a single entry by Ian Musgrave published on May 25, 2008 7:39 AM.

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