Alternate post title: Why Charles Jackson is a tool who can quote papers, but doesnt understand what he is reading.

I get this question all the time, and its totally valid:

How do you tell the difference between an endogenous retrovirus that is shared because of common descent, and a retrovirus that was endogenized independently in two species?

A follow up paper to the one I wrote about here (Me, and you, and Zaboomafoo) provides a lovely example of how we do this!

So heres the back story: There are a ton of different retroviruses. Its not one big homogeneous group of ‘virus kind’, each family of retrovirus has its own genetic features and personality quirks. For a nice comparison so you all can appreciate the diversity of retroviruses: you are as ‘related’ to green algae, as HIV-1 is ‘related’ to a family of ERVs, HERV-K.

Lentiviruses, like HIV-1, apparently dont like to endogenize very much. Weve looked in humans, primates… we cant find any. We found one in a particular species of bunnah. And they just found another one in Cheirogaleus medius, a kind of lemur.

Neato!

Well, another lab looked at different species and genera of lemur… and found another endogenous lentivirus! In another genus of lemurs, Microcebus! Additionally, these lemur ERVs are 93-96% similar to one another, while HIV-1 viruses are only 80-85% similar to one another, max.

At the surface, this might make it look like Microcebus and Cheirogaleus share this ERV because of an endogenization event in a common ancestor– ‘same virus’, two different genera. Right?

Wrong!

You need to remember that where retroviruses insert in a genome is random. Like Ive said a hundred times before, yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts– near which active genes, exactly which nucleotides are up/down stream, is random.

However, there is no complete ‘lemur’ genomic sequence. How can you ‘tell’ where an ERV has inserted if you dont even have a genomic map?

PCR!

To identify putative lentiviral ERVs in lemur genomic sequences, Gilberts lab compared the RELIK sequence to lemur sequences (however little we have). Areas where the sequences matched, they called putative lentiviral ERV sites. Even if you dont have complete lemur genome sequences, you can still see what sequence is directly upstream and downstream from the ERV. In this drawring I made, A is a ‘normal’ sequence, B is the sequence after an ERV has inserted, and C is what happens when an ERV ‘pops out’– the pink parts, the viral LTRs (promoters) line up during cell division, and the gene portions of the ERV just pop out, leaving a ‘solo LTR’ footprint of where the complete ERV used to be.

Because Gilbert knew what sequence was upstream and downstream of the LTR, he could design primers specific for that location, and PCR amplify that region of the lemurs genome. IF there was not and had never been an ERV at that site in the genome, he expected a 250 base pair product. IF there used to be an ERV there, and there was only a solo LTR left (which is what he thought he saw in his RELIK/genome comparisons), he expected a 670 bp product (just an example, he did a few this way).

You can see how different these sizes look in a gel in Figure 5.

He determined that even though the lentiviral ERV sequences were super similar, they are not located in the same genomic regions. ‘Present’ PCR fragment sizes in Microcebus species were ‘absent’ fragment sizes in Cheirogaleus (he also tested this in a similar, but different way, Southern Blots, and other basic molecular genetics tools– Im not explaining them in this post, lol).

He found that with every test, with this particular family of ERVs, there were no orthologous sites of insertion. By using molecular clocks, Gifford determined that though this lentivirus endogenized in two different genera, it happened at about the same time– about 4.2 million years ago. Thus it can be found in the same location in various species of the genus Microcebus, meaning common descent. However it is in a different location in species of the genus Cheirogaleus, meaning Microcebus/Cheirogaleus infections were two independent events.

We can differentiate between common descent and two independent events.

And they didnt even need a complete ‘lemur’ genomic sequence to figure this out.

Comments

  1. #1 William Wallace
    April 13, 2009

    Pete, you asked several questions, and I answered most of them. I am not able to answer your last question as stated, could you elaborate?

    Albatrossity, I do read biology papers from time to time, and would read more if the ones I wanted to read were free and readily accessible. As it is, I have to ask biology professors to send them to me.

    I’ll have to take your word that biology letters almost always have an alternative explanation for the observed facts. I have not noticed that pattern in the non-biology journals I’ve read.

  2. #2 William Wallace
    April 13, 2009

    One other point, Albatrossity, I fell for your “observed facts” goal post shift, and actually quoted it. The example I was using was questioning an assumption used to draw conclusions about observed data.

    Short of a letter alleging a paper fudged data, observed facts are not usually challenged, are they, Albatrossity?

  3. #3 Shrunk
    April 13, 2009

    WW: This sort of thing has been attempted, e.g., Dodd’s 1989 fruit fly paper describing her observations, but the best they could do as far as I understand it was generate more fruit flies. Sure, population A could eat Starch based food, while population B could eat maltose based food, and ~80% of the females surveyed from population A preferred to mate with males from population A, while only ~20% of the females surveyed from population A would bother to mate with males from population B. But they were all still fruit flies capable of and even willing to breed with one another.

    Well, if you think about it, this is not that surprising. Consider we are 6 millions years removed from our MRCA with chimpanzees. If you assume a generation time of 25 years for humans, vs 2 weeks for fruit flies, that means for fruit flies to achieve the degree of divergence we have from chimps would require over 9000 years. So if you’re correct that an 80% degree of speciation has already been achieved with fruit flies, I’d say that’s already way ahead of schedule.

  4. #4 Shrunk
    April 13, 2009

    WW: I like the video, too bad it is sullied by Dr. Jackson’s error in assigning the Morganucodon to the permian layers instead of the triassic.

    I see you like the video so much, you’ve now made it “private.”

  5. #5 William Wallace
    April 13, 2009

    Using your numbers, I get ~41,500 years.

    Your definition of speciation is strange. If you think mating preferences (as opposed to actual cross fertility) defines a species, you have a point. One of the problems with the word species…biologists keep changing what it means. Which is why I referred to novel, tangible features.

    Some bacteria divide every 15 minutes from what I understand. Using your 6E6 and 25 numbers again, I get 6.8 years for divergence as great as what you claim in chimps and humans.

    P.S. Based on early screening results, the film has evolved. See http://www.youtube.com/watch?v=sF2Aa_SudC0 (Morganucodon: Evolutionism versus Creationism) if you want to learn about the great rat grandmother evolutionists claim you have.

  6. #6 Albatrossity
    April 13, 2009

    WW

    You were claiming that you did not have to provide an explanation for observed facts (homologous sites of ERV insertions in chimp and human genomes). Your distinction (“The example I was using was questioning an assumption used to draw conclusions about observed data”) is therefore irrelevant. In a typical example, author A details some observations and makes a conclusion about the explanation. Author B sends a letter to the journal saying that the observations, which are assumed to be correctly reported, can be explained in some other way.

    That’s what I am asking you to do. You have the same observations as we do. The conclusion of those who did the work is that common descent is the best explanation. I’ve asked you several times for your explanation, but you don’t have one. By default, then, the explanation (common descent) that was proposed by the original authors is still the best one at this time.

    Case closed, at least until you manage to give us an alternative explanation for those observations.

  7. #7 Pete
    April 13, 2009

    Pete, you asked several questions, and I answered most of them. I am not able to answer your last question as stated, could you elaborate?

    I’m not sure what is not clear about the question, though I can see it was worded a bit funny. I assume you know what a nested hierarchy is. Biologists assert that, for instance, they have identified many shared ERVs that aren’t just shared among primates but fall into a nested hierarchy. In your post I thought you seemed to imply that no such pattern existed, we can talk about whether that is true later. I think it is unless the data I have seen is completely fabricated. But skipping that discussion, for the sake of argument I want you to assume that indeed the ERVs fall into a nested hierarchy. Likewise, I want you to assume that Abbie could demonstrate that ERVs will not only insert themselves in one location but will pick randomly from many possible locations, say up to 100. If these two things were shown to you (1: they are in a nested hierarchy and 2: there is some randomness in viral insertion), would this be evidence for common descent?

  8. #8 William Wallace
    April 13, 2009

    I am not a biologist, but the case is not closed in my estimation. From what I can gather, the conclusion you stand behind is based on assumptions not yet backed up by good scientific evidence.

    But from what you’ve given me….

    Possible explanations for homologous sites of ERV insertions in chimp and human genomes:

    1. Under the assumptions: that ERV insertion sites are random or at least stochastic enough (note the biologist’s mathematical ambiguity here); that homologous ERV integration sites cannot possibly be coincidental in two different species; that ERV markers really came from some long ago RV infection at just the precise instant necessary (just so); that extrapolated genetic clocks work, and have always worked, ah, like a clock, within a specified margin of error; and so on and so forth….common descent.
    3. Latent functionality. Latent in either the sense of not currently known or not currently active.
    3.a. For example, an occult (in the clinical sense) checksum, CRC, hash, programmer signature, or comment of some sort.
    4. And one of my favorites: Coincidence.

    But I could speculate all day. Speculation is pointless. Show me the data. I don’t have data. For example, I don’t have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random, such as demonstrating a cause/effect relationship between a known random source, such as thermal noise, to ERV insertion point outcomes, and also backed up by an analysis of ERV site selection to show that it is likely stochastic, e.g., using the NIST/Florida State University Diehard battery test suites to test for randomness), etc.

  9. #9 Pete
    April 14, 2009

    Possible explanations for homologous sites of ERV insertions in chimp and human genomes:

    I much more interested in the nested hierarchy of ERV insertions that creates the same phylogenetic tree for primates already established by other molecular evidence, namely figure 4.4.1 on this link (I’m sure your familiar with the link)

    http://www.talkorigins.org/faqs/comdesc/section4.html#retroviruses

    You might need to cut and paste that, I don’t know how to post links. Comparing shared ERVs between humans and chimps is one thing, but when an entire nested hierarchy is created going back as far as new world monkeys, then any other explanation besides common descent, which explains this figure exactly, would have to be rather creative. And yet, this data is widely known so there must be some explanation by creationists. Even if insertion sites weren’t random, that wouldn’t explain why the insertions we have fall into this nested hierarchy. There would be no reason why a specific new world monkey species might not share one with humans and no primate “in between” (the standard phylogenetic tree). If these were found, indeed if we never found any sort of nested hierarchy because these were abundant, of any molecular data much less ERVs, I would consider common descent to be falsified, and indeed never would have been persuaded of its truthfulness in the first place (until several years ago I was a creationist.)

  10. #10 Stephen Wells
    April 14, 2009

    Willy, willy, you yourself cited a couple of papers showing retroviruses inserting at any one of _thousands_ of places. In order for you to deny common descent you need to show that typically retroviruses only insert at _one_ place. So your position is already falsified. How much simpler could this be?

    By the way @dmso74, “learn some population genetics” was not intended as snark, it was an honest piece of advice. Sorry if it came across snarky. The stuff Shrunk pointed you at is, well, some population genetics :)

  11. #11 Shirakawasuna
    April 14, 2009

    Wallace likes to pretend that each scientific question operates in a bubble as well – it makes it easier for him to be in denial of the facts. I say so because he’s doing it at the moment – despite the *facts* that there are recorded ERV insertions all over the genome in various species, smack dab in the middle of SINEs and other areas, he instead demands a comparison with noise (which, by the way, the data should match pretty well if he were to actually look at it). That is, despite the fact that ERVs will insert in many different areas with widely divergent functionality/essentially no nucleotide-specific functionality, he likes to pretend that there’s still some latent pattern that can’t be excluded, as if it would allow him to avoid the probability argument (it doesn’t).

    It’s all very sad.

    Also, why is it that the people having difficulty with this stuff say that the *only* way an identical insertion point of the same ERV is by common descent? That’s not the argument at all: it’s that the probability of a fairly random ERV insertion happening in that same place over and over and over again, just happening to form a nested hierarchy, is quite unlikely. Instead, common descent explains this pattern of *inheritance* very nicely and it already well-proven in its own right.

  12. #12 windy
    April 14, 2009

    But I could speculate all day. Speculation is pointless. Show me the data. I don’t have data. For example, I don’t have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random

    If you had bothered to read as far as Table 1 in the paper you cited in #32 (getting the first author’s name wrong, too), you would have noticed that different experiments with the same viral vector produce different integration sites. The integration sites are in the NCBI database, so you are free to check the data if you don’t believe them.

    For example, an occult (in the clinical sense) checksum, CRC, hash, programmer signature, or comment of some sort.

    Does that programmer sneak into cell cultures to comment on ongoing experiments?

  13. #13 Albatrossity
    April 14, 2009

    WW

    Thanks for finally addressing the question. It’s interesting that you can talk endlessly about stuff, and yet finally admit you haven’t read a single primary paper on the subject…

    As for your explanations, here’s my analysis.

    1) Common descent – most likely, and, as others have mentioned, most consilient with lots of other observations.

    2) you seem to have skipped this one.

    3) Latent functionality – I’m going to proceed without your definition of that term, even though I know that is a dangerous move, since semantic games are your specialty. But there is no evidence for this at all. Can you provide an experiment to test this hypothesis?

    4) Coincidence – incredibly unlikely from these data alone, and made even more incredibly unlikely by the consilience of the other data (e.g. chromosome 2 fusion, globin genes, GULO gene, etc.). As others have mentioned, the nested hierarchies in this case have been tested innumerable times, and have basically held up every time.

    If you really wanted the data, you could find it. Do a google science search for “erv chimp human genome” and dig up the papers. Go to a decent library with a subscription to the Web of Science and do the same search. Get the free papers online (like this one) and get the rest via interlibrary loan. The folks who generated those papers have done a hell of a lot of work. You can do a little work yourself and get their papers to see if they really have overlooked all of your amateur disagreements with their conclusions. That really is how science works, at least in the real world.

    Or you can remain true to form and sit on internet forums sniping at stuff that you don’t really understand.

  14. #14 William Wallace
    April 14, 2009
    I don’t have, as requested in [#5], a cite to a scientific paper that found, and not just assumed, good scientific evidence that ERV sites are random

    you would have noticed that different experiments with the same viral vector produce different integration sites.

    And you think that is good evidence? Pinewood derby racetracks with different inclines will produce different race times for a given set of pinewood derby cars, but that doesn’t establish randomness, or even let you know how much randomness affects race times. Indeed, there is some randomness in a pinewood derby race time even if the incline is not changed, but other factors also explain differences in race times, such as lubrication wearing out, different orientations of the pinewood derby car from race to race, the moment of inertia, the center of gravity, which lane you’re on, etc. You cannot attribute the entire distribution of race times in a pinewood derby race to randomness until you specifically target and attempt to characterize what effect randomness has on a race, and what effect other factors have on the race.

    Meanwhile, Albatrossity shoots down the a restaurant critic for not being a world class cook, (as though you need to be a cook to be a good restaurant critic), I’d like to paraphrase an audience member from the debate:

    Is there a single, published scientific paper that concludes, and not just assumes, that ERV integration points are stochastic?

  15. #15 Stephen Wells
    April 14, 2009

    Willy, willy, willy, you yourself have cited papers showing that these viruses randomly insert at any one of thousands (at least) of points. Didn’t you _know_ that’s what you were citing?

  16. #16 Stephen Wells
    April 14, 2009

    Oh, and willy: albatrossity is not telling the critic he needs to be cook. He’s telling you that it would help if you could at least use your cutlery correctly and not try to eat your own shoes.

  17. #17 Eric Saveau
    April 14, 2009

    Another way of looking at the “restaurant critic” analogy failure – Of course the critic doesn’t need to be a cook, but he would be in much better position to criticize if he actually spent some time eating at the restaurant! Merely reading a copy of the menu from the restaurant’s website and talking to some other people who dislike the restaurant – most of whom also never ate there – means his supposed criticisms are baseless.

  18. #18 Shrunk
    April 14, 2009

    WW:

    3127 insertion points and not a single repeat? Yes, I consider that good evidence for random insertion. Remember, this study was specifically looking for evidence of non-random insertion and reported some preference for particular types of sites (active vs inactive sites), but not to the point that specific sites are targeted. So, yes, that’s a conclusion, not an assumption. If they had found those 3127 insertions were limited to, say, the same five or six specific sites, instead of 3127 completely different sites, then they would have concluded that insertion is not random and, furthermore, that ERV’s can no longer be used as evidence for common descent. They didn’t find that, so random insertion and ERV’s as evidence for common descent is confirmed. Are you really so dense you can’t understand this?

  19. #19 Pete
    April 14, 2009

    3127 insertion points and not a single repeat? Yes, I consider that good evidence for random insertion.

    This would not be evidence for pure randomness. But it is evidence that the ERV does not insert itself into the same spot, or even one of merely 1000 spots. Though I’m sure if they tried an 3128 insertions, they would probably get 3128 spots, lets be conservative and assume that the most we know is that the ERV will insert itself into a spot with odds 1/3127. If chimps and humans share one, that is unlikely, but not terribly so. But what if chimps and humans share 5 such ERV insertions. Now we are at (1/3127)^5. And yet, humans and chimps share much more then just 5. But that is not the best evidence, as I tried to make clear in my last post. The best evidence is that when we consider other primates, including gorillas, orangutans, etc, not only do we find they share ERVs in homologous locations, but when they are shared, the fall into a nested hierachy. If we find an ERV we share with a new world monkey in a homologous position, the nested hierarchy pattern we find and indeed the prediction of common descent is that we will find it in every creature we share a more recent common ancestor with as well. That is what we find, exactly this nested hierarchy, once again as evidenced by figure 4.1.1 on
    http://www.talkorigins.org/faqs/comdesc/section4.html#retroviruses

    I would like to know from Mr. Williams an alternate explanation for this nested hierarchy.

  20. #20 windy
    April 14, 2009

    Indeed, there is some randomness in a pinewood derby race time

    Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, motherfucker?

    You cannot attribute the entire distribution of race times in a pinewood derby race to randomness

    Apparently you have forgotten what ERV said in the original post

    Like Ive said a hundred times before, yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts– near which active genes, exactly which nucleotides are up/down stream, is random.

    She did not attribute the entire distribution of race times to randomness. But thanks for flogging that strawman for us once again.

  21. #21 windy
    April 14, 2009

    argh, “entire distribution of race times” should have been “entire distribution of insertion sites”

  22. #22 Eric Saveau
    April 14, 2009

    Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, motherfucker?

    Aaaaand Windy wins this thread.

  23. #23 William Wallace
    April 14, 2009

    The foul mouthed Windy wrote:
    Is there a single, published scientific paper that concludes, and not just assumes, that there is some randomness in pinewood derby race times, [deleted]?

    Foul language aside–this is a great question. Let my answer serve as an example to Abbie, who still hasn’t answered [#5].

    It turns out that Dr. Scott Acton (Physics Ph.D./Texas Tech University–same school as the infamous Dr. Michael Dini) has studied the physics of the pinewood derby in painstaking detail. Furthermore, he has even put out a video summarizing his results, and it is also a useful example of the scientific method.

    This video would be great for some ERV readers, because in it, he teaches about characterizing and isolating variables, coming up with and testing hypothesis, performing simulations, and, best of all, characterizing the magnitude of random effects.

    He did it in a way that a 7 year old could understand (my 7 year old son understood it), so it might be a bit challenging for some ERV fans.

    But take a gander at Physics and the Pinewood Derby.

    (And no, my son did not win the Pinewood Derby, but that is because he built the car himself, and was not allowed to take full advantage of the conclusions presented in the video, as they were beyond his dexterity. He did pretty well, though, considering he’s 7.)

    …you yourself have cited papers showing that these viruses randomly insert at any one of thousands (at least) of points. Didn’t you _know_ that’s what you were citing?

    You mean the paper that Abbie first wrote about, and in which the authors observed that there was a _bias_?

    3127

    Please, see [#5], where I preemptively addressed this issue.

    3127 different sites don’t matter. A completely deterministic process can result in 3127 different outcomes.

    And while assuming that a random model as a basis of scientific reasoning and investigation can be justified in some situations, it is not good evidence that the random model is an accurate reflection of reality.

    I’ve already given examples, from quantization error, to rolling a die to see if it is fair, to illustrate why a model that might be useful in one application is not necessarily a reflection of reality.

    In order to provide good scientific evidence that a random model is an accurate representation of a physical process, you need to specifically investigate this, isolating all of the other variables that you are able to isolate.

    Pete, I’ll process your reasoning, give me some time. Meanwhile, do you know of a paper that concludes that ERV insertions are not deterministic, but stochastic, and doesn’t just assume they are stochastic?

    To anybody:

    Once again, I’d like to paraphrase an audience member from the debate:

    Is there a single, published scientific paper that concludes, and not just assumes, that ERV integration points are stochastic?

  24. #24 Pete
    April 15, 2009

    Mr. Wallace,

    Thank you. Please do explain the nested hierarchy of ERV insertions. Who knows, you might actually convince me. I was open minded enough to be convinced that common descent was true, after 28 years of life and at least 14 years of being an active creationist, so it is clear my mind can be changed by evidence. But since this pattern is clearly explained by common descent, I’m going to need a very very good explanation for what other explanation could explain it (apart from the God made it that way to test my faith explanation).

  25. #25 William Wallace
    April 15, 2009

    Pete, I am going to do a mathematical analysis under various assumptions for you. I’ve started looking at your figure. Do you know how many ERVs are known to exist in human DNA? If you could provide a cite, all the better.

  26. #26 William Wallace
    April 15, 2009

    Nevermind, I’ll just assume Abbie’s figure of 98,000 is correct.

  27. #27 William Wallace
    April 15, 2009

    Pete, (or anybody else) is this a fair representation of the data we are talking about?

    P.S. Mark Chu-Carroll, speak now or forever hold your peace.

  28. #28 Stephen Wells
    April 15, 2009

    Willie, since we’ve established that retroviruses _typically insert at any one of a large number of sites_, your entire argument already failed. We know _we can’t predict where a given insertion will happen_ and _ it could happen at any one of many places_; your own cites establish this, so you don’t get to argue against it. All you’re left with is arguing about whether the universe is deterministic or not; which is unknowable and irrelevant.

  29. #29 Shrunk
    April 15, 2009

    I think a crucial point is being overlooked here (by one of us, that is.) No one is claiming that retroviral insertion is an entirely stochastic process. As Abbie wrote above, “…yes, some like to insert near active genes, and some like quiet genes, but exactly where a retrovirus inserts– near which active genes, exactly which nucleotides are up/down stream, is random.”

    The only point of dispute is whether retroviruses have “preferences” for specific sites sufficient to result in every single primate having ERV’s at those sites, without invoking common descent at the most likely explanation. As I’ve said before, at a bare minimum we need at least a single documented example of two independent yet identical retroviral insertions before we can begin to consider this hypothesis as even a remote possibility. To date, WW has yet to provide even a single such instance, so his hypothesis is a complete non-starter. Arguing that retroviral insertion is not completely stochastic is irrelevent, because we’ve already concluded that to be the case. What is lacking is evidence that the deterministic nature of retroviral insertion is sufficient to produce universal fixation of identical ERV’s in unrelated species. (And, yes, this doesn’t even yet address the issue of nested hierarchies that Pete has raised, and that WW is only now starting to “process” despite having expounded on this topic as nauseum for how long now?)

    Another issue that has been ignored: Abbie has cited this paper in her “Creationist Claims about ERV’s” post:

    http://www.genetics.org/cgi/content/full/158/2/769

    Now, most of this paper admittedly goes over my head. But from what I can understand, the authors were able to identify two separate retrotransposon insertions that occurred at the exact same site that occurred 12 million years ago. IOW, even if identical separate insertions had occurred, it is possible to detect this. To me, that clearly demonstrates that ERV’s as evidence of common descent is not just an assumption, but an empirically verifiable conclusion.

  30. #30 cprs
    April 15, 2009

    1. It would be helpful to have a definition of nested hierarchy,
    and I would hope for something more specific than this: http://evolution.berkeley.edu/evosite/lines/IVDhierarchies.shtml

    If anyone’s read Michael Denton’s critiques of evolution you’ll appreciate how this is precisely the ground from which he argues, in fact talkorigins arguments about cytochrome c (4.1, a few sections above their dated review of ERVs cited here several times) are the very substance of the argument he uses against both gradualism and common descent. I’m sure by using LTR comparison & other methods of dating, by showing the inverse correlation between insertional and sequence polymorphism, the nature of the nested hierarchy for ERVs can be shown to be more refined, but it would be nice to see a definition concisely in print. It would of course assume all ERVs are exogenous in origin, and involved in complex host function by fortuitous accident.

    2. (minor point) WW, please correct old world monkey spelling in your data table.

    3. CERV 1 or PtERV1 family.
    Abbie’s interesting Frankenstein post explores reasons for lack of human infection with CERV1 – but is hardly illuminating on the problem of a lack of human orthologues for CERV 1 (most of its insertions of course are not ‘orthologous’). The problem is accentuated by the date for CERV1 being calculated at older than the divergence date for man and chimp. Perhaps the clock is not so reliable?

    How does one explain the report from the paper I cited that at least 6 human apparently orthologous sites were deleted without trace?

    More troubling, how does one explain that the same six orangutan sites were deleted without trace(assuming orangutans share a common ancestor with chimps, baboons and humans)?

    The authors address this implication by claiming 2 of these sites were homologous insertions with the same insertion sites and not orthologous, because of BP differences between macaques and chimps. That does sharpen the question of how confidently one can distinguish the two phenomena – Abbie’s primary issue for this thread.

    The same problem applies also to the CERV2 family. This is not a single recombination/deletion but 2 site losses from different branches of the evolutionary tree for both humans and orangutans.

    I don’t doubt a good explanation can be conjectured, and I welcome reading them, but it does suggest the case for common descent from ERVs proves too much.

  31. #31 Stephen Wells
    April 15, 2009

    IIRC Denton attempts to critique evolution because he thinks that bacterial genes should be more similar to worm genes than they are to human genes. He is wrong, for obvious reasons.

  32. #32 Shrunk
    April 15, 2009

    cprs:

    I’m not sure what you’re failing to understand with the CERV 1 data. As the paper says itself:

    Our data support a model where ancestral chimpanzee and gorilla species were infected independently and contemporaneously by an exogenous source of gammaretrovirus 3–4 million years ago.

    That seems clear and simple. Humans and orangutans don’t possess the ERV because we were never infected by the virus in the first place.

    I’ve already offered an explanation of the CERV 2 findings above (which was based on an email correspondance with the paper’s authors; you might want to try addressing your questions to them). It again touches on the issue of population genetics. If you research the meaning of “most recent common ancestor”, you will find that not all of that ancestor’s genes are passed on to all it’s descendents. That is obvious; if they were passed on, we would all be identical clones. In the subsequent divergence of the human and chimp species from that ancestor, many genes were lost, and CERV 2 appears to have been among them. That’s my, admittedly less than expert, understanding of the issue.

    You’re still displaying a fundamental misunderstanding of the ERV evidence. The emergence of a specific ERV in a genome is the result of a series of extremely unlikely events, so the existence of the same ERV at the same site in two different species is far far more likely the result of common descent than of those unlikely events occurring in the exact same way, down to the smallest detail, in the ancestors of those two species. Extend that to, not just two species, but several in a perfect nested hierarchy, and the odds become even longer. That there are differences in ERV’s between species does nothing to refute this.

    I have no idea what your section on nested hierarchies means, so I won’t respond to it, other than to point you to this excellent video on the subject (He makes the script available in case he speaks too quickly for you to follow).

    http://www.youtube.com/watch?v=5MXTBGcyNuc&feature=channel_page

  33. #33 William Wallace
    April 15, 2009

    Stephen Wells, which is the latest post [#128] applied to?

    Shrunk [#129] wrote:

    The only point of dispute is whether retroviruses have “preferences” for specific sites sufficient to result in every single primate having ERV’s at those sites, without invoking common descent at the most likely explanation. As I’ve said before, at a bare minimum we need at least a single documented example of two independent yet identical retroviral insertions before we can begin to consider this hypothesis as even a remote possibility.

    Apply different standards, much?

    First, how could two independent yet identical RV insertions possibly be shown? If it met your criteria, based on the rather mathematically imprecise “stochastic enough” assumption, you would simply declare that they were not independent insertions.

    Second, assuming even stronger evidence were found, say, an identical insertion found in orangutans and humans, but not chimps, evolution would be declared the winner here too with something like “Big deal. Natural selection creates that sort of stuff everyday.”[1]

    That is, if such a result were likely to ever see the light of day.

    But let’s assume that:

    1. A researcher finds an ERV in humans and orangutans, but not gorillas and chimpanzees.
    2. Let’s assume she writes a paper titled “no so fast, evolutionary explanatory filter.”
    3. Let’s assume it actually gets published in a “peer reviewed scientific journal” (because we all know how much biologists love seeing evidence against evolution).

    How long before calls for the anonymous peer reviewer names to be released are made; how long before surreptitious campaigns orchestrated by the NCDE against the journal editor in charge are waged; how long before Abbie Smith and others in the PT-mafia start calling the researcher “creationist, Christian, anti-science, data fudging hobo”?

    Third, why the different standards? On the one hand, you claim proof of common descent based on ERV and assumptions of random insertion points, but on the other, you know that you would not accept as falsification of this view data indicating a common ERV in humans and orangutans but not chimps.

    This is how biology is done, but not science.

    Footnotes
    [1]Beware the believers (@ 0:28)

  34. #34 Pete
    April 15, 2009

    Mr. Wallace,

    I can only guess what your graph is supposed to be reporting, perhaps you could give me a source (or did you create it from the figure I sent?)

    For a good discussion of nested hierarchies, start with this link
    http://www.freethoughtdebater.com/FEvolutionCase.htm
    which itself is an intro to the separate and converging lines of evidence for common descent. Just a warning, since you guys are undoubtedly Christian, you will probably be offended by a few things this guy says. This is a clear introduction to the evidence of common descent, so I wish the author would remove the snarkyness.

  35. #35 Pete
    April 15, 2009

    Second, assuming even stronger evidence were found, say, an identical insertion found in orangutans and humans, but not chimps, evolution would be declared the winner here too with something like “Big deal. Natural selection creates that sort of stuff everyday.”[1]

    I would find this strong evidence against common descent. Has such an insertion been found? It would still need to be explained why the rest of them our found in a nested hierarchy. If ERVs do insert in identical locations, I would expect to find no pattern among species. We should see some shared by humans and orangutans but not chimps/gorillas, some shared by chimps, new world monkey, and dogs, but not foxes, old world monkeys, and orangutans, some shared between humans, mice, and turtles, but not any other reptile or mammal, etc. Ie, there shouldn’t be a nested hierarchy at all.

    I don’t think your hypothetical researcher would have any problem if the data could be reproduced.

  36. #36 William Wallace
    April 15, 2009

    Pete, it was from your TO link. I thought it was rather self explanatory. Each of the Ei for i=1 to 14 were the 14 ERVs in the TO link.

    Which brings up a question for Abbie: There are 11 common ERVs listed at TO. You mention 14. Is the TO link old news? Please understand that not all of us are ERV graduate students, and that this is an honest question.

    Pete, please provide a single source for me to analyze. Even if it is a scientific paper (I can get access to them, it’s just not convenient–but in this case, it would be preferred, because evolander sites have been known to mischaracterize scientific research.). If you must synthesize multiple papers to justify your viewpoint, so be it….send me cites for all of the scientific papers directly related and commenting on ERV and common descent.

  37. #37 Pete
    April 15, 2009

    evolander?

  38. #38 jon
    April 15, 2009

    @pete#137:

    As in EVOLANDER! COME OUT EVOLANDER! WE HAVE YOUR WOMAN!

    WW is a modern day analog to Malachi in Children of the Corn…blindly following charismatic religious leaders against all evidence.

  39. #39 Pete
    April 15, 2009

    Hmmmm, I originally learned about ERV insertions from “Coming to Peace with Science” by Falk. Since then I have seen the information reprinted in various forms across the web, and I believe Abbie has a description of it here on her blog. But I think the TO link itself explains it pretty well, and provides references for all of its claims. Following their own link, the figure itself comes from the following paper.
    Lebedev, Y. B., Belonovitch, O. S., Zybrova, N. V, Khil, P. P., Kurdyukov, S. G., Vinogradova, T. V., Hunsmann, G., and Sverdlov, E. D. (2000) “Differences in HERV-K LTR insertions in orthologous loci of humans and great apes.” Gene 247: 265-277.

    Props to you if you actually go out and find this paper. I’m much to lazy for that. I find it a fairly reasonable assumption that if this paper did not in fact report a nested hierarchy of ERV insertions and TO is simply lying about it, someone would have pointed that out. It is nearly 10 years old now.

  40. #40 brandon
    April 15, 2009

    Jon, I had the same exact impression. Coinages are tricky things. They can make one look like a buffoon if one doesn’t take care.

  41. #41 Albatrossity
    April 15, 2009

    Ahh, the true WW character comes out in #133. First off, he has repeatedly avoided the question in #113 –

    Latent functionality – I’m going to proceed without your definition of that term, even though I know that is a dangerous move, since semantic games are your specialty. But there is no evidence for this at all. Can you provide an experiment to test this hypothesis?

    Secondly, he sets up a fantasy situation, with damaging data that he fervently wishes could be found, and acts as if it was real. His fantasy is complete with evil conspiratorial scientists suppressing data, and all the other trappings of the paranoid mindset that characterize his entire online persona.

    Finally, he beats his favorite dead horse, that biology is not really science. Iin his tiny world, only math (and maybe physics) can be designated as science.

    Those latter two are not useful additions to the thread, WW. If Biology is Not Science, why are you wasting your valuable time here? Particularly after you admit that you have read none of the relevant papers? Is it because it is beneath you to read those scummy biology papers? Perhaps if you had read those papers, and understood them without the creationist blinders, you would be able to propose a useful hypothesis to test one of your coincidental notions.

  42. #42 Shrunk
    April 15, 2009

    WW:

    Apply different standards, much?

    First, how could two independent yet identical RV insertions possibly be shown? If it met your criteria, based on the rather mathematically imprecise “stochastic enough” assumption, you would simply declare that they were not independent insertions.

    I’m sorry, I thought you just had a slightly less than adequate understanding of what we were discussing. I didn’t realize you don’t even have the slightest fucking clue.

    Demonstrating identical RV insertions would be trivially easy. That study we keep talking about? The one with the 3127 RV insertions? Suppose those were not found at 3127 distinct sites, but at 3126. That would mean two of them were at identical sites. Are you following so far? Suppose they were only distributed among 6 different sites. That would be very strong evidence that retroviruses target specific sites, and would essentially kill the ERV argument for common descent (though if this were true, then I can’t see how a nested heirarchical pattern could result).

    Do you follow what I’m saying now? To support your argument, it is not enough to say that RV’s tend to insert in certain general regions of the genome. We already know that they do. But to support your argument, you need to demonstrate that RV’s will target, not certain parts of the genome, or even specific genes, but specific base pairs. In order to demonstrate this, you must find at least one example of an RV inserting into the same base pair in two individuals. Do you know of such a case?

    If you have two separate ERV’s at two distinct sites, those have resulted from separate insertions. It doesn’t matter whether they are a single base pair apart, or located on entirely different chromosomes.

    Do you get it now? If not, maybe you can ask your seven year old to explain it to you.

    But let’s assume that:

    1. A researcher finds an ERV in humans and orangutans, but not gorillas and chimpanzees.
    2. Let’s assume she writes a paper titled “no so fast, evolutionary explanatory filter.”
    3. Let’s assume it actually gets published in a “peer reviewed scientific journal” (because we all know how much biologists love seeing evidence against evolution).

    How long before calls for the anonymous peer reviewer names to be released are made; how long before surreptitious campaigns orchestrated by the NCDE against the journal editor in charge are waged; how long before Abbie Smith and others in the PT-mafia start calling the researcher “creationist, Christian, anti-science, data fudging hobo”?

    Are you even paying attention? We’ve been talking about almost exactly that just above (true, it’s an ERV in common with chimps/gorillas and missing from humans/orangutans, but close enough). You’ll note that none of your predicted responses have arisen from that paper. Although in this case, the differences resulted from infection after the process of speciation had begun, in general common descent does not predict that ERV’s, like any other allele, will not be lost as the process of speciation continues. Remember genetic drift?

    Not all of the differences between us and chimps need have resulted from mutations. Some are just different alleles from the common ancestor that have been retained in one line, but not the other. However, the identical genes indicate common descent. Think of it: Might there be some genes that your brother inherited from your grandfather that you did not? Does this mean that you and your brother don’t share a common ancestor? However, if there was a new mutation that had developed in your grandfather that you and your brother shared, that would be sufficient to prove you and your brother having been descended from him regardless of whatever genetic differences there may be between the two of you.

  43. #43 cprs
    April 15, 2009

    First Pete and Stephen, isn’t it wiser to be familiar with the arguments of your critics and not caricature them? Denton’s case (and though he was early affiliated with DI he is no longer, and is not a creationist in any ordinary sense) is that genetic and protein sequences correlate closely with physiological and anatomical similarities, no big surprise – it emphatically doesn’t show lineal descent – a typological critic of Darwin in his own day if he could access it would use the molecular biological data to make his case against ‘the Origin’. Denton was driven to his sceptical conclusions by the data, despite the storm of anger and loss of reputation he knew he’d face. He used a nested hierarchy for cytochrome c sequence differences to ilustrate his case. That’s why Pete your falsification implies a lack of appreciation of how your opponents think.

    ERV nested hierarchies however are different and more interesting because they’re considered exogenous in origin.

    I’ll read the pages you recommend (thanks for the gentle forewarning, Pete) – but dealing with blasphemy, mocking and inanities on sites promoting evolution is all too familiar – sadly it reveals much more than is intended.
    Convergent evolution, alluded to so often at freethought, is masterly tautology – read a little of the tortuous history of psychoanalysis and you’ll realise afresh the dangers of a overly plastic theory. Alone it’s little more than black magic.

    Shrunk, I have of course read the two groups of authors’ interpretations of their findings CERV 1 and 2, but the data they cite indicates homologous ERV insertions which do not match the evolutionary tree, they would usually be called orthologues – but aren’t here, they’re attributed to cross infection. That’s precisely the problem.

    I follow the pop gen and genetic drift arguments, but why should both orangutans and humans lose all the apparent ‘orthologues’ of both large families, that does seem convenient reasoning.

    As to the challenge about identical insertion sites for different ERVs – isn’t Abbie’s own example sufficient?

    WW for reference the two main sources I’ve been using are both freely accessible, here they are again:

    http://genomebiology.com/2006/7/6/R51
    http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.0030110

  44. #44 cprs
    April 15, 2009

    Abbie’s example of course is here:
    http://www.genetics.org/cgi/content/full/158/2/769

  45. #45 Shrunk
    April 15, 2009

    At the risk of being a blabbermouth, there’s one other point I’d like to make. When Pete says:

    I would find this strong evidence against common descent. Has such an insertion been found?

    I respectfully suggest this shows a misunderstanding of the nature of the ERV evidence. As has been mentioned, evidence of this type has been found, but is not evidence against common descent. ERV’s cannot be used to falsify CD; they can only be used as evidence in its favour. The most creationists can do is demonstrate some mechanism besides CD that could explain identical ERV insertions arising in different species. However, that would still not disprove common descent.

    What ERV’s do accomplish is to completely, finally and utterly falsify the “hypothesis” (if it may be dignified with the term) that humans are the result of a separate act of creation, and not related to any other species. In other words, while ERV evidence is not necessary to prove common descent, it is sufficient. That’s what Abbie means when she says, “if Darwin and Wallace decided to open a resort and spa in Cuba instead of going into science, if every fossil was still hidden– The second we found ERVs, common descent would have smacked us in the head like a sack full of doorknobs.”

  46. #46 Shrunk
    April 15, 2009

    As to the challenge about identical insertion sites for different ERVs – isn’t Abbie’s own example sufficient?

    OK, so there we have it: One single example of an identical insertion (Which the investigators were incidentally able to distinguish as two separate insertion events)out of how many hundreds of thousands of ERV’s going back at least 30 million years. So, can someone really good at math calculate whether this is sufficiently “non-random” to explain every single individual human, chimp, orangutan and gorilla having ERV’s at exactly the same site? Or should we just go with my gut feeling that the answer is “Not a chance.”

  47. #47 David Marjanović
    April 15, 2009

    Braveheart,

    you seem to have overlooked that science cannot prove, only disprove. That’s what the principle of parsimony exists for.

    Let me simply repeat comments 70 and 72. Either you provide evidence that retrovirus insertion is not random, or you give up and accept that repeated insertion in the same places in a single consistent tree-shaped pattern is astronomically financially unlikely, so unlikely it can be safely dismissed several billion times over.

    Let’s assume that ERV insertion really is random. then the logical inference is that ERVs shared by common descent must have come from an endogenization event in ONE individual. then all, for example, chimps and humans are descendents of that one individual ancestor. and this must hold true for all ERVs shared at the same genomic location in different species. I am no expert, but it seems like these shared ERVs are pretty numerous, meaning that all the species that share them also came from one individual. does this not strike anyone else as a bit hard to swallow?

    No, why?

    Ever heard of Mitochondrial Eve and Y-Chromosome Adam? That’s how it works. Just more slowly in most cases – but time is always available.

    Albatrossity, if what you say is true, scientific journals would only publish letters critical of papers if the letters also posited alternative explanations. If scientist A wrote a letter merely pointing out how an assumption, made in a paper written by scientist B, taken to its logical conclusion would produce a paradox, for example, under your understanding of “science” said letter would not be published as it puts forth no alternative explanation.

    Forgive me if I don’t believe you. Indeed, it seems to me that journal editors would favor response letters that analyzed the paper in question, and did not try to sneak in alternative ideas via the letter route, as opposed to vetting those alternatives through the more formally peer reviewed paper path.

    WW

    P.S. This is a blog, not a journal.

    Erm…

    1) It seems to me that you believe there’s a difference between “paper” and “letter” in scientific journals. But there isn’t (except that “Letters” have three pages in Nature, “Articles” have five, and “Brief Communications” have about one). All of these are papers, and all of these are therefore peer-reviewed. If I’ve correctly interpreted what you mean, you don’t live in the same world as the rest of us.
    2) There aren’t different kinds of science in blogs vs journals. Science is science. I mean, what did you think!?! That you’re allowed to get away with arguments from ignorance and personal incredulity because this here is a blog!?!

    the permian layer

    In just three words, you have revealed profound ignorance on geology and on stratigraphic nomenclature. Congratulations.

    <headshake>

    There isn’t just one layer per period (really, how did you imagine sediment deposition? Did you ever imagine it at all!?!), and period names are capitalized…

    Regarding your other point, I am not convinced of macro evolution. I would be convinced if a repeatable experiment were devised to create a new species.

    Define “species”.

    I’m completely serious. There are at least 25 different definitions in the literature, and depending on the definition there are between 101 and 249 endemic bird species in Mexico. Please pick one.

    This sort of thing has been attempted, e.g., Dodd’s 1989 fruit fly paper describing her observations, but the best they could do as far as I understand it was generate more fruit flies.

    <headdesk>

    “Fruit fly” is a term like “mammal”. Under any definition there are thousands of species of fruit flies.

    <headdesk>

    TSIB.

    One of the problems with the word species…biologists keep changing what it means. Which is why I referred to novel, tangible features.

    Define “novel”, “tangible”, and “feature”. Sorry if that sounds like I’m nitpicking; I’m not.

    […] if you want to learn about the great rat grandmother evolutionists claim you have.

    <headdesk>

    Look. I could understand if you called it a shrew. Sure, it’s as far away from shrews as it is from rats, humans, whales, and so on, but at least it hasn’t got gnawing teeth and the jaw musculature and head shape that go along with this.

    You mean the paper that Abbie first wrote about, and in which the authors observed that there was a _bias_?

    A bias that doesn’t come anywhere close to favoring single nucleotides over their neighbors.

    When people say ERVs are inserted in the same place, they mean the same place, not a stretch of 10 or 100 nucleotides.

    3127 different sites don’t matter. A completely deterministic process can result in 3127 different outcomes.

    Then suggest one. Or Ockham’s Razor will get you.

    P.S. Mark Chu-Carroll, speak now or forever hold your peace.

    Huh? What makes you think he’s reading this thread?

    ~:-|

    Finally, he beats his favorite dead horse, that biology is not really science. Iin his tiny world, only math (and maybe physics) can be designated as science.

    Which is funny, because math is not a science. It consists of definitions and tautologies; “1 + 1 = 2″ is true because of the ways the symbols “1″, “2″, “+” and “=” are defined. It only uses internal contradictions to disprove ideas, not physical reality the way science does. Math is necessary for science, but it isn’t a science itself; it’s math.

  48. #48 David Marjanović
    April 15, 2009

    If you have two separate ERV’s at two distinct sites, those have resulted from separate insertions. It doesn’t matter whether they are a single base pair apart, or located on entirely different chromosomes.

    And if you have the same ERV at two distinct sites, those have resulted from separate insertions of the same retrovirus. Here, too, it doesn’t matter whether they are a single base pair apart, or located on entirely different chromosomes.

    BTW, I highly recommend this paper (pdf).

  49. #49 Anton Mates
    April 15, 2009

    WW,

    3127 different sites don’t matter. A completely deterministic process can result in 3127 different outcomes.

    It doesn’t matter whether the process is completely deterministic. As long as it produces lots of insertions at lots of different sites, and almost never produces two insertions of identical ERVs at the same site, ERVs can be used to map common descent.

    Similarly, an evolutionary program which creates “mutations” via a decent pseudorandom generator can have effectively identical performance to that of a program which reads in “genuinely” random numbers from a Geiger counter or something. “Deterministic” vs. “indeterministic” is a total red herring hee; -any natural process might be deterministic or indeterministic in principle. We can never tell for sure, and evolution doesn’t care.

  50. #50 Anton Mates
    April 15, 2009

    total red herring hee;

    er, “here.” What I get for fixing typos without hitting preview.

  51. #51 Pete
    April 15, 2009

    Denton’s case (and though he was early affiliated with DI he is no longer, and is not a creationist in any ordinary sense) is that genetic and protein sequences correlate closely with physiological and anatomical similarities, no big surprise – it emphatically doesn’t show lineal descent -

    Denton now fully accepts common descent. I haven’t read his latest book but since I agree with his concept of God created (via evolution) I doubt I would have much I disagreed with him.

    I respectfully suggest this shows a misunderstanding of the nature of the ERV evidence. As has been mentioned, evidence of this type has been found, but is not evidence against common descent.

    Okay, your right, let me rephrase. Its not evidence against common descent. But it would (does?) weaken the evidence the ERV markers do evidence common descent. Because they do so BECAUSE they are in a nested hierarchy pattern in this would be showing that they weren’t. If we found them in common among many different animals clearly out of the phylogenetic tree will would build based on other evidence, then they would not be evidence for common descent. And actually, now that I have returned to proof read this paragraph, they might cause common descent doubt unless we could show they were not random insertions at all and the very point of much of this post is demonstrating they insert in many different locations. Since we know that is true, if we found the orthogoulous (sp) ones in a scattered pattern, we would lots of explaining to do.

    But now you saying such a case exists, one that exists in both gorillas and chimps but not humans (not sure why orangutans are mentioned since that is an earlier branch so one can conclude the infection hadn’t happened yet, unless an even more distant primate also has it?). For the chimp/gorilla but not human insertion I guess you are positing that after the insertion happened when we were homochimporillas, but it wasn’t yet fixed in our population when the gorillas branched off, nor fixed in our population as homochimps when the chimps branch off, but later became fixed in the first two and was lost in us? Sorry, that was a mouthful.

    Convergent evolution, alluded to so often at freethought, is masterly tautology

    I don’t think covergent evolution is overly plastic. If one started showing evolutionary convergence all the way down on the level of exact genetic base pairs, located in very distinct species but nothing in between, I would think that was too much coincidence for common descent to be true. But indeed, it is that the convergence is superficial that makes it not weaken the case of common descent but strengthen it. In the classic example of whale fins vs fish fins, we converge on a fin shape but only superficially, the whale is a modified walking mammal. We discovered it was a mammal for other reasons which then predicts those fins are modified mammal arms and hands and sure enough, pull back the skin and you find all the same mammal bones. If it wasn’t superficial, indeed if bats, which are clearly mammals on all other traits, had bird wings, ie modified reptile arms, as opposed to modified mammal arms (or really long fingers in this case), that would be evidence of direct design to me and not common descent.

  52. #52 David Marjanović
    April 15, 2009

    orthogoulous

    Orthologous.

    For the chimp/gorilla but not human insertion I guess you are positing that after the insertion happened when we were homochimporillas, but it wasn’t yet fixed in our population when the gorillas branched off, nor fixed in our population as homochimps when the chimps branch off, but later became fixed in the first two and was lost in us?

    That’s entirely possible.

    Another possibility is that the ERV was cut out in the human lineage; but in that case there should be a solo LTR (see purplish rectangle in the figures above), and I don’t know if there is.

  53. #53 Shrunk
    April 15, 2009

    I’m afraid I may have caused more confusion than anything else with the discussion of CERV 1 and 2 (though in my defense, I’m not the one that brought them up).

    Here’s the paper in question:

    http://genomebiology.com/2006/7/6/R51

    As can be seen, it discusses CERV 1 and 2 which exist in chimps and some other primates, but not humans. However, there is no mention of the precise location of any of the insertions, presumably because these haven’t been sequenced yet. Although, AFAIK, the distribution of these ERV’s remains a bit of a puzzle, they don’t affect the evidence for common descent at all, which is based on ERV’s in identical locations. Sorry for any confusion.

  54. #54 William Wallace
    April 15, 2009

    Shrunk [#145] wrote: ERV’s cannot be used to falsify CD; they can only be used as evidence in its favour.

    It’s good to see you admit this. And it is sadly not surprising. The evolution racket is an unfalsifiable ratchet. Evidence in support of evolution gets collected, prized, and trumpeted, and evidence against is ignored because it doesn’t matter.

    Pete, did you get that? Still convinced? They’re whispering sweet nothings in your ear, and you’re changing your stance as a result.

    You could find 11 other ERV insertions that do not support the nested hierarchy you’ve been talking about, and it wouldn’t matter I guess. I suspect that 111 ERV coincident insertions not supporting common descent with 11 supporting wouldn’t matter either.

    Not being able to falsify common descent means that tracking and reading ERV integration sites to support common descent is a metaphysical pursuit, and not a scientific pursuit (viz. a viz. CD, to reiterate the point.)

  55. #55 William Wallace
    April 15, 2009

    vis-a-vis, whatever.

  56. #56 Tyler DiPietro
    April 15, 2009

    “It’s good to see you admit this. And it is sadly not surprising. The evolution racket is an unfalsifiable ratchet.”

    Saying that one particular phenomenon wouldn’t falsify common descent is not the same thing as conceding that common descent is unfalsifiable. You’d be able to make this distinction, if you were not a retard.

  57. #57 LanceR, JSG
    April 15, 2009

    Evolution is easily falsifiable. See here for a brief overview.

    If you knew anything about evolution, instead of your strawman delusions, you would already know this.

    Of course, I’m betting that you *do* know it, and you’re just another Liar for Jesus.

    Unrelated, cprs can kiss my atheist ass. Blasphemy is only blasphemous to believers. Reread ERV’s tagline again. Only twits who have no actual arguments to make whine about “incivility” and “blasphemy”. Real arguments get heated. You should listen in to actual scientists discussing actual science sometime.

  58. #58 Pete
    April 15, 2009

    Mr. Wallace,

    I certainly think common descent is falsifiable. But regardless, I encourage you to continue to explore another explanation for the nested hierarchy of ERVs insertions, at least the ones from the diagram that has been linked several times. From my angle, even if the viral insertions always hit the same location (which they obviously don’t, we know of at least 3127 from a study of 3127 attempts) that still wouldn’t explain why they fall into a nested hierarchy. Common descent explains it exactly.

  59. #59 windy
    April 15, 2009

    It turns out that Dr. Scott Acton (Physics Ph.D./Texas Tech University–same school as the infamous Dr. Michael Dini) has studied the physics of the pinewood derby in painstaking detail. Furthermore, he has even put out a video summarizing his results, and it is also a useful example of the scientific method.

    I had a feeling that you were going to pull something like that with your pinewood derby example. But guess what, a video is not a published scientific paper! Man, even when you’re setting a rhetorical trap, you get it wrong.

    (Imagine the indignant whining if, in response to Willy-Wally’s request for a peer-reviewed scientific paper, someone tried to offer him some amateurish video! Oh my!)

    And from the webpage, looking at a section called “change and luck”, it appears that they assume that a certain amount of the variation in race times is due to chance and luck!

    3127 different sites don’t matter. A completely deterministic process can result in 3127 different outcomes.
    And while assuming that a random model as a basis of scientific reasoning and investigation can be justified in some situations, it is not good evidence that the random model is an accurate reflection of reality.
    I’ve already given examples, from quantization error, to rolling a die to see if it is fair

    Rolling a die, even a fair one, is physically a largely deterministic process. So your standards seem to be changing from one paragraph to the next.

  60. #60 Pete
    April 16, 2009

    Real arguments get heated. You should listen in to actual scientists discussing actual science sometime.

    Real arguments might get heated, I don’t think that makes it a good thing. Why would real scientists be uncivil to each other? Perhaps us humans are destined to always been angry and insulting but I think at least it would be an ideal that debaters focused on the issues and go light on the personal comments.

  61. #61 William Wallace
    April 16, 2009

    I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

    Enough said on this thread.

  62. #62 Stephen Wells
    April 16, 2009

    Willy bails, still not understanding anything, apparently astonished that things falling can be considered as evidence for but not against gravity.

  63. #63 Shrunk
    April 16, 2009

    I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

    Enough said on this thread.

    And I knew, as I wrote that, that there was an excellent chance you would misconstrue it and quote mine it to support your argument. Still, if I pitched everything I wrote to your droolingly encephalitic level of comprehension, there would be no point in having any discussion here at all.

    Did you not notice this part of my post as well?

    What ERV’s do accomplish is to completely, finally and utterly falsify the “hypothesis” (if it may be dignified with the term) that humans are the result of a separate act of creation, and not related to any other species. In other words, while ERV evidence is not necessary to prove common descent, it is sufficient.

    An analogy: In investigating a robbery, the presence of the suspect’s fingerprints at the crime scene is very strong evidence that he is guilty. The absence of fingerprints, however, does not mean he is innocent. Fingerprints can only confirm his guilt, they cannot falsify it.

    If you disagree with me, provide a hypothetical example of an ERV pattern that would be impossible with common descent.

  64. #64 Albatrossity
    April 16, 2009

    Echoing what Shrunk said, it is noteworthy that WW ignored the rest of that comment in order to quotemine the single sentence that resonated with his presuppositions.

    Even more noteworthy would be an unpacking of this sentence: I do want to sincerely and without snark thank Shrunk, whomever he or she is, for the disclosure that ERVs can be considered as evidence for but not against common descent.

    Given multiple opportunities, WW has failed to even whiff at designing a hypothesis to test his notions. So not only is there no evidence FOR special creation of humans, and plenty of evidence AGAINST it, there is not even a hypothesis which would allow us to test this notion. WW is a master at applying very strict standards to the conclusions of others, but consistently and spectacularly fails to apply those same standards to his notions.

    Please come back when you have a hypothesis which will allow you to generate evidence FOR special creation, WW. Which will be, as we all know, never.

  65. #65 Shrunk
    April 16, 2009

    Carrying the analogy of the crime scene a bit further:

    Let’s suppose in this robbery there are multiple lines of evidence that point to a particular suspect as being guilty. There are several reliable eyewitnesses that confirm seeing the suspect break into the building. Surveillance cameras capture images of him entering thru a window, then leaving moments later with a heavily laden bag across his shoulder. The suspect has signed a detailed confession, including information that could only be known to the perpetrator of the crime. Samples of his DNA are recovered from the crime scene. After all this evidence has been gathered and the suspect charged and imprisoned, fingerprints are also found at the crime scene that perfectly match the accused’s.

    Knowing what a tight spot he is now in, the accused hires that crack criminal defence lawyer, William Wallace.

    Come the trial, and Wallace is now cross examining the police detective. Ignoring all the other evidence, he goes directly to the fingerprints.

    “Now, officer, you are pretty certain those fingerprints belong to my client. Just what makes you so sure?”

    “Well, we recovered several prints from the scene that perfectly matched those from the accused.”

    “How do you know this was not a coincidence? How do you know the actual criminal was not someone whose fingerprints just happened to match my client’s?”

    “That would be impossible. Everyone’s fingerprints are unique.”

    “Oh? And how do you know this? Do you believe that fingerprints are determined by completely random processes?”

    “Well, not completely random, no. There are some patterns of whorls and such that tend to occur in many individuals. But this does not change the fact that every fingerprint is unique and can be distinguished from from anyone else’s. No one has ever come across fingerprints from two different people that were identical.”

    “And you consider that sufficient reason to believe the prints from the crime scene are my client’s? You believe this even though you have not examined the fingerprints of every single person alive to make certain that, in fact, no two prints are alike. Is that correct?”

    “Yeah, pretty much.”

    “Well, thank you for your honesty. I guess the jury can decide whether they consider that sufficient reason. Now, these fingerprints seem pretty important to your case, don’t they?”

    “Well, there is all the other evidence. The eyewitnesses, the videotape, the DNA, the signed confession. Those are already pretty persuasive. But I guess the fingerprints are nice to have, too.”

    “So, tell me this, officer: If you did not have the fingerprints, would you still believe my client was guilty.”

    “Yeah, sure.”

    “Now, I’m going to ask you this one more time: Are you saying that, even if there were no fingerprints, you would still have sufficient evidence to convict my client?”

    “Yeah, that’s pretty much the case.”

    “AH HA!” Wallace exclaims, looking about the courtroom with a triumphant expression.

    The jury and audience stare back, glassy eyed and incredulous, and the judge says, “Mr. Wallace, exactly how much are you getting paid for this?”

  66. #66 David Marjanović
    April 16, 2009

    Why would real scientists be uncivil to each other?

    Why would real scientists care about civility at all (one way or another)? Civility is not an argument. :-|

    A bit more autism, please.

  67. #67 Pete
    April 16, 2009

    Why would real scientists care about civility at all (one way or another)? Civility is not an argument. :-|

    But surely there is a difference between arguing about the evidence, and calling each other names.

  68. #68 Pete
    April 16, 2009

    Mr. Wallace,

    Its your right if you don’t wish to comment on this thread any longer. But I do think you need to take some time to “process” what it means for the ERV insertions to fall into a nested hierarchy. Given the insertions are an actual event in history, could not likely insert into the same place (probably not even 1 time, much less all the virus shared by so many species), but most importantly fall into a nested hierarchy pattern, I think the conclusion is inescapable. So inescapable that Answer in Genesis has to take the route of denying they are virus’s at all. Indeed, it seems any person, group, or creationist organization that comes to understand the data as observed has had to take this stance, because if ERVs are viral insertions then they clearly evidence common descent. Whether it is possible they are not viral insertions, well I’m not a biologist. But it is clear they look so much like viruses that Answers in Genesis, instead of just assigning them some random genetic function, has admitted their relationship to viruses, but they conclude that the ERV are not insertions, but that Viruses themselves COME from the ERVs. I’ll let you chew on the plausibility and theology of such a hypothesis.

  69. #69 William Wallace
    April 16, 2009

    Pete,

    I’ll be donig a post on ERVs soon enough. Maybe you can stop by and chat then. Since ERVs cannot be used to falsify common descent, it isn’t a scientific test of the theory of common descent. Again, enough said, really.

  70. #70 Shrunk
    April 16, 2009

    Since ERVs cannot be used to falsify common descent, it isn’t a scientific test of the theory of common descent.

    I guess that’s debatable. If something is able to produce irrefutable evidence for a concept, I would say it is a scientific test, even if it is not able to falsify the concept. However, what is beyond debate is that ERV’s are able to falsify the notion that human beings are not related, by descent, to other organisms. Since the ideas of common descent and special creation are mutually exclusive, and there is no third option between the two, by falsifying one idea, ERV evidence it is able to confirm the other as correct.

    If you’re going to be quoting this thread in your article, be sure to include that. Otherwise, you would be deceptively quote- mining, and I’m sure you don’t want to do that.

  71. #71 Pete
    April 16, 2009

    Mr. Wallace,

    I disagree with you. But whatever. When you do make that post, please explain what ERVs are, and why they are in a nested hierarchy pattern. Any time I hear someone comment on them without mentioning the nested hierarchy, I take it as a complete non-answer and evidence they do not actually understand what the evidence is they are trying to refute.

    Thanks,
    Pete

  72. #72 Shirakawasuna
    April 16, 2009

    Wow, how idiotic. No, Willy, DATA tends not to be falsifiable unless it was actually fraudulent or incompetently gathered. Falsifiability has to do with theories, hypotheses, etc. If we had ERVs in the genome and knew that they were inherited, by common descent we would expect them to form a nested hierarchy. If they didn’t, we’d have to rethink the scenario, perhaps leading to falsification. The multitude of data in support of common descent wouldn’t disappear if ERVs had conflicted with it, so it would all be weighed in kind.

    Naturally, the data actually does support common descent and the prediction was thus (of course) supported. Falsification, as I listed above, was entirely possible, although not in the silly sense you seem to ascribe to it.

    Might want to work on that poor middle school textbook understanding of the scientific method, WW. Then again, I don’t remember even the most useless of texts confusing data for theory.

  73. #73 Shrunk
    April 16, 2009

    Maybe I should explain my thinking in saying that ERV’s can only confirm, not falsify, common descent.

    In trying to imagine the scenario that would be least consistent with CD, I came up with one essentially the same as what Pete described above (#135). That would be an arrangement whereby common ERV’s are scattered in a chaotic, random matter among various species with no evidence of any pattern of inheritance or nested hierarchies. It would be as if each species just reached into a grab bag of random ERV insertions. Any two species could have a number in common just by luck, but it would not have any bearing on their phylogenetic relationship.

    Now, suppose we actually observed this. Would it falsify common descent? I don’t see how it would. All it would demonstrate was that common ERV insertions can occur in unrelated individuals without having been inherited from a common ancestor. It would certainly be a puzzling finding, and would falsify many of our accepted theories regarding the nature of ERV’s. But it would not be evidence against common descent. It would just mean ERV’s could not be used as evidence for common descent.

    Does this make sense to everybody here?

    As a side note, the kind of chaotic pattern of ERV insertions is what would be expected if WW’s “theory” of non-random retroviral insertion were true. Since we don’t observe it, this is strong evidence, if any more were needed, that his ideas are wrong.

  74. #74 Yeshivish Atheist
    April 16, 2009

    Shrunk,

    What if we observed ERV data and used it to construct a nested hierarchy which completely contradicted the current nested hierarchy we have now based on other evidences, such as comparative DNA. It would mean that our older lines of data which out current theories of common descent are based on would be contradicted by the ERV data, no?

  75. #75 Shirakawasuna
    April 16, 2009

    Shrunk, I don’t think falsification doesn’t work like you think it does. When one comes upon data that conflicts with the prediction of a well-established theory, that is, one that has been quite predictive and is supported by a lot more data, you don’t just immediately chuck it: you start thinking of explanations. That old data doesn’t disappear, the entire idea isn’t just thrown out.

    Now, in the case of physics sometimes this *does* happen, largely because the realities they are dealing with, while often confusing, are much simpler. That simplicity allows them to have greater certainty with negative results. Other fields don’t have this luxury, dealing with more complicated scenarios, so interpretation and weighing evidence becomes more difficult.

    The basic point I’m making is that if ERVs were found to have a different but consistent nested hierarchy, it would cast doubt on common descent. It wouldn’t immediately ‘falsify’ it without further study because one would still have to contend with the huge amounts of supportive data.

  76. #76 Stephen Wells
    April 16, 2009

    @174 is probably right; an ERV nested heirarchy which produced groupings like ( walrus , ( spider , artichoke ) ) and ( fruitfly , ( cholera , televangelists ) ) would be a bit of an issue.

    Thus we snatch the straw from drowning Willie’s grasping hands once more :)

  77. #77 Anton Mates
    April 16, 2009

    Shrunk,

    Since the ideas of common descent and special creation are mutually exclusive, and there is no third option between the two, by falsifying one idea, ERV evidence it is able to confirm the other as correct.

    At least one of those premises is false, though. Special creation is mutually exclusive with common descent if sufficiently narrowly defined, but there are tons of other options. Multiple centres of divine creation, beloved by many biologists of Darwin’s day; multiple lineages of organisms arising naturally on Earth via independent abiogenesis or panspermia events; and so forth.

    Creationists like to claim that mainstream evolution and special creation are the only possible options, ergo any “weaknesses” of the first hypothesis are strong evidence for the second, but that’s just their lack of imagination talking.

    That would be an arrangement whereby common ERV’s are scattered in a chaotic, random matter among various species with no evidence of any pattern of inheritance or nested hierarchies. It would be as if each species just reached into a grab bag of random ERV insertions. Any two species could have a number in common just by luck, but it would not have any bearing on their phylogenetic relationship.

    Now, suppose we actually observed this. Would it falsify common descent? I don’t see how it would. All it would demonstrate was that common ERV insertions can occur in unrelated individuals without having been inherited from a common ancestor.

    I think the implications would be more serious than that. If each one of these ERVs was found across a whole species, or across a large chunk of a species, then it would appear to have been inherited from a common ancestor. And by measuring modern insertion rates or constructing molecular clocks, we could conclude that germ-line ERV insertions are quite rare (on a human time-scale); again, this would suggest that most observed ERVs have been inherited from the carrier’s distant ancestors.

    So we would have ERV-based patterns of common ancestry at the population and species levels, but not above that–just as if each species were independently created. This would be strong evidence against common descent, unless we could develop a good explanation of why ERV-based phylogenetics would suddenly fail above the species level.

  78. #78 Shrunk
    April 17, 2009

    OK, guys. You’ve convinced me. I hadn’t thought of the possibility of a series of nested hierarchies that suggested multiple, independent lines of descent (What the creationists would call “microevolution within kinds”). While such a finding would be very difficult to reconcile with all the other evidence for universal common descent, taken on its own it would be better explained by creationism than by evolutionary theory.

    So, to WW: This is probably of little relevence, since if you actually plan to write an article on this, you would obviously base it on more than an anonymous blog comment by someone with no known qualifications in the field. But just for the record, I no longer maintain that ERV evidence cannot falsify common descent.

  79. #79 cprs
    April 17, 2009

    Shrunk,
    I was the ‘culprit’ who raised the CERV 1 and 2 families. The 2006 Genome study is based on a chimp whole genome search, as even the abstract explains, it identifies orthologues which requires determining their respective chomosomal positions, unless I have missed something major. So why claim otherwise? I am completely mystified by your statement.
    ‘Of the 42 families of chimpanzee endogenous retroviruses identified in this study, 40 were found to have orthologues in the human genome, including 9 that were identified in this study for the first time [14] (see Additional data file 1). Two previously identified chimpanzee endogenous retrovirus families do not have human orthologues (Table 2).’

    There is a serious problem here for common descent, though by no means insuperable.

    As to Pete and other comments on convergent evolution, I don’t think you have begin to grapple with the depths of the problem with the cursory nod towards fins, here’s a short catalogue, http://www.thegreatstory.org/convergence.pdf. The collector is Darwinist, as her seamless but revealing extrapolation to human thought illustrates. Just ask the question, if these parallels had arisen in closely related branches, wouldn’t they vindicate a (non existent) common descent? Look again at the highly similar tertiary structure for haemoglobin and myoglobin, ancient paralogs they are often called, but have you considered how their primary sequence shares only 6 or so amino acids out of about 140? There are many other examples.

    As to poor old Denton, I am not surprised he has retracted his originally trenchant and wide ranging critique under the furious storm of personal attacks. No mild agnostic likes to be attacked as a campaigning creationist, when he isn’t. Here’s a short section from Nature’s Destiny to show his current view, “The design of living systems, from an organismic level right down to the level of an individual protein, is so integrated that most attempts to engineer even a relatively minor functional change are bound to necessitate a host of subtle compensatory changes. It is hard to envisage a reality less amenable to Darwinian change via a succession of independent undirected mutations altering one component of the organism at a time.” He’s become a kind of mystical Lamarckian.

    As to the danger of personal invective in science – I am surprised anyone who knows how such tactics hindered Lister, Harvey, Koch or a host of other pioneers has the courage to advocate such obscurantist tactics here. Ad hominems usually reveal more about their authors than their targets.
    I also acknowledge, though, with all due respect to our mathematical colleagues, it’s perhaps not the only obscurantist tactic used on this thread.

  80. #80 William Wallace
    April 17, 2009

    This is probably of little relevence, since if you actually plan to write an article on this, you would obviously base it on more than an anonymous blog comment by someone with no known qualifications in the field. But just for the record, I no longer maintain that ERV evidence cannot falsify common descent.

    Interesting, thanks. So now we have something important to talk about, and I have more work to do.

    Before I begin, at the talkorigins (TO) link in [#109], why were the rightmost three ERVs included in Figure 4.4.1? At first blush, it appears to be a form of deceptive presentation of data, but perhaps I am missing something. I mean, humans have more than 14 ERVs, and more than 3 ERVs not shared by the chimps et. al, right?

    On a related note, Common ERVs is in my view an objective and better presentation of data than what is in the TO link at [#109]. It is presenting essentially the same data, leaving the implications of the hierarchy as an exercise for the reader. It even preserves ERV 12 through 14 (E12 through E14, though I don’t know what makes 12, 13, and 14 any more important than E15 through E90000.

    The TO presentation could be further improved with horizontal error bars representing best estimate of the time the RV is thought to have become endogenous, +/- uncertainty, and best estimate of time species were thought to have split, +/- uncertainty in time and species definition, all indicated.

    Anyway, how would I go about finding as much information as I can about all known ERVs in the six species of animals and one species of humans trumpeted at Talk Origins, including the ERVs not listed in [#109]‘s Figure 4.4.1?

    I’d like to perform a mathematical analysis of data if such sequences exist in some database.

    I’d also like a knowledgeable evolutionist to help perform an analysis and also construct some simulations. The simulations will of course be based on assumptions, and I want to come up with a reasonable set of assumptions, and also disclose them, and perhaps allow them to be tweaked so that various simulations can be performed.

    Assuming this hasn’t been done before (and it may have, which could save a lot of time), I think it would be a useful exercise to think about various possibilities.

    Next, assume that, for the sake of argument, the species indicated in the “Common ERVs” (my representation) row headings are randomly permuted, and the ERV indices are now numbered 15 through 28.

    Suppose a third chart is constructed by again randomly permuting the row headings, and numbering the indices 29 through 42.

    And now, we will have, hypothetically, three different nested hierarchies (NHs) that could be constructed, one of which will support CD, and the other two, equally compelling, which would not, assuming the permutations resulted in a sufficiently different row order from the CD supporting E1 through E11.

    Certainly, it seems to me, this sort of data would cause people like Abbie to rethink, at the very least, the theories about how ERVs end up at their current locations. But would it give any evolutionist pause to rethink CD?

    Now, this hypothetical example could be taken further, with a variety of outcomes. For example, suppose that the strongest single NH supports CD, and the current tree of life, but two other only slightly weaker NHs of 10 common ERVs per nested hierarchy support two, drastically different from the first NH, of 10 common ERVS each, say E20 through E29 supporting NH2 and E30 through E39 supporting NH3.

    Extending this example further, at what point does the nested hierarchy trumpeted by TalkOrigins [#109] become the equivalent of finding a shape in a cumulus nimbus cloud that strongly resembles Frosty the Snowman?

    Shrunk, are you a biologist? A professor? An ERV researcher? Perhaps you could help me shine some critical light on the ERV evidence of CD.

  81. #81 James F
    April 17, 2009

    For crying out loud, William Wallace thinks the universe is 6,000 years old. ERVs are the least of his concerns.

  82. #82 cprs
    April 17, 2009

    Dear William,
    being none of the above, I offer a small start. There are at least 42 common ERV families in primates (CERV 1 and 2 are both lacking in man in orangutans), details in Genome reference Shrunk links again, Table 2.

    CERV 2 for example in your table would be -(humans) +(chimps) +(bonobos)+ (gorillas) – (orangutan) +(macaques) – new world monkeys. The text cites 6 apparently orthologous sites, but many are not shared by all species, (Table 5)

    CERV 1 would be 0(humans), 5(96)(chimps), ?(bonobos), 3(81) (gorillas), 8(81) baboons, 0(orangutan), 8(46)(macaques).
    The numbers are apparently orthologous (total including non-orthologous sites), but there are qualification about the precision of the determination and the paper doesn’t specify between which species the sites are deemed orthologous.
    Taken from, http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054887&rendertype=table&id=pbio-0030110-t002

  83. #83 windy
    April 17, 2009

    I was the ‘culprit’ who raised the CERV 1 and 2 families. The 2006 Genome study is based on a chimp whole genome search, as even the abstract explains, it identifies orthologues which requires determining their respective chomosomal positions, unless I have missed something major. So why claim otherwise? I am completely mystified by your statement.

    I think you are missing something. The 2006 study does not identify orthologous insertion sites between chimps and other apes that are lacking in humans.

    As you noted above, the PLoS study they cite was able to unambiguously identify “95.8% of the insertions occur at non-orthologous regions”. But what about the other 4.2%?

    Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous

    So they were not identified as having identical insertion sites, they were identified as inserting within the same 160,000 base pair region! That’s still quite a lot. Some of these “overlap” loci were shown to be non-orthologous at a closer look, and some couldn’t be pinpointed to an exact location because of the repetitive sequence.

    These two articles you cited are a little unclear at points, so I don’t blame you for being a little confused. When they say things like ‘the age of this virus family is inconsistent with the age of the human chimp split’, they are just using it as a build up so that a couple of sentences later they can jump out of the bushes and go ‘A-HA! This is how we resolve the inconsistency!’ My old professor would have told them that a scientific article does not need to be a detective story…

    ‘Of the 42 families of chimpanzee endogenous retroviruses identified in this study, 40 were found to have orthologues in the human genome, including 9 that were identified in this study for the first time [14] (see Additional data file 1). Two previously identified chimpanzee endogenous retrovirus families do not have human orthologues (Table 2).’
    There is a serious problem here for common descent, though by no means insuperable.

    It simply means that the retrovirus infections that created these two families occurred after the human-chimp split. These CERV families occur in other primates, but not at identical insertion sites to the chimps.

    The 2006 article also says that “two CERV 30 (HERV K10) insertion polymorphisms have been identified in human populations”. So, some humans have insertions that others lack. That is not a problem for common descent of humans, it simply means that some insertions are more recent than others.

  84. #84 cprs
    April 17, 2009

    Thanks Windy, most CERV1 insertions aren’t orthologous and there’s doubt about those that are – agreed. However there are at least apparent 12 hot spots for a number of common insertion sites between nonhuman primates, that alone is noteworthy, and the exact insertion site would be interesting to know.

    Again there are apparently orthologous non human primate sites for CERV2 – there’s a bit of brinkmanship as you suggest – and one is definitely whittled away, but there are up to six sites mentioned. None is specified except the representative one, and that by chromosomal locus not by sequence. I agree the non orthologous sites for these two families and CERV30 are irrelevant to descent, but just as they cite the CERV30/HERVK10 orthologue as indicative of human chimp ancestry, so the blemishless deletion of up to six orthologous sites of CERV2 is remarkable for the same reason.

    Who’s going to write to the authors?

  85. #85 cprs
    April 17, 2009

    Of course, I’m not suggesting they already have the answer to hand (maybe they do after 3 years) – merely to encourage its pursuit. Sorry re double post – was interrupted.

  86. #86 Anton Mates
    April 17, 2009

    cprs,

    However there are at least apparent 12 hot spots for a number of common insertion sites between nonhuman primates, that alone is noteworthy, and the exact insertion site would be interesting to know.

    But those intervals don’t seem to be common insertion sites—they were in the “ambiguous”category to start with, and the authors were able to shoot down four of them as non-orthologous. The rest remained ambiguous, but the authors provide additional lines of evidence as to why they’re probably not orthologous either.

    I agree the non orthologous sites for these two families and CERV30 are irrelevant to descent, but just as they cite the CERV30/HERVK10 orthologue as indicative of human chimp ancestry, so the blemishless deletion of up to six orthologous sites of CERV2 is remarkable for the same reason.

    No one is suggesting that they were deleted, though—in fact, the authors specifically say they weren’t. Shrunk’s suggestion, which s/he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. Then there would be nothing to delete–humans would be descended from members of that ancestral population which never had those ERVs.

    Who’s going to write to the authors?

    How about you? It sounds like they’re happy to talk about this stuff.

  87. #87 windy
    April 17, 2009

    But those intervals don’t seem to be common insertion sites—they were in the “ambiguous”category to start with, and the authors were able to shoot down four of them as non-orthologous. The rest remained ambiguous, but the authors provide additional lines of evidence as to why they’re probably not orthologous either.

    Right! That’s what I was trying to explain in #183, but this is a shorter and clearer way of saying it.

    No one is suggesting that they were deleted, though—in fact, the authors specifically say they weren’t. Shrunk’s suggestion, which s/he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. Then there would be nothing to delete–humans would be descended from members of that ancestral population which never had those ERVs.

    No, this is not consistent with the article at all (and I don’t see where shrunk says anything about corresponding with the authors?). If there were ancestral polymorphisms at several integration sites of these ERVs, why would all of them have been lost by genetic drift in humans, but not in chimps? And particularly CERV 2 is way too old to have been maintained as an ancestral polymorphism up to the chimp-human split.

    I think the authors are trying to get across the idea that these ERV families are likely the result of multiple exogenous infections in chimps, by emphasizing how unlikely the alternative is.

    PS. It’s worth looking at Figure 1 in the 2006 paper. Look at what sequences cluster closest to the CERV 1 and 2 families – there’s a baboon virus, a feline virus, and our old friend the PERV! It doesn’t seem unlikely that these virus families could have come to chimps via horizontal transmission.

  88. #88 Shrunk
    April 18, 2009

    A couple comments:

    First of all, I did mention corresponding with the authors of the paper. I’ve been able to find the reply I received, which was rather brief, but to the point:

    “Our findings are not incompatible with evolution. Transposable elements can be lost from (or added to) lineages over evolutionary time.”

    I have emailed the author again to inform him of this thread. I’ll let you know if I receive a reply.

    Second, the main point that seems to be overlooked here is that only ERV’s found at identical locations (i.e. to the exact base pair, not just chromosomal regions or “hot spots”) are relevent as data regarding CD. ERV’s located at different locations are from separate insertion or transpositional events, and are not of any phylogenetic relevence. In this paper, I see no explicit mention of identical insertion sites for any of the ERV’s.

    Thirdly, since it seems to be a matter of some discussion, I’m a male. :)

  89. #89 windy
    April 18, 2009

    Thanks Shrunk, I somehow missed the bit about the correspondence. But I think the authors are not referring to ancestral polymorphisms, but indels and new insertions after the human-chimp(s) split, to explain the differences.

  90. #90 cprss
    April 19, 2009

    Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term ‘orthologues’ is presumptive only, and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved – the argument cuts two ways.

  91. #91 Anton Mates
    April 19, 2009

    windy,

    If there were ancestral polymorphisms at several integration sites of these ERVs, why would all of them have been lost by genetic drift in humans, but not in chimps?

    I imagine the polymorphisms could have assorted geographically. The ERVs we’re talking about belong to just two families, after all, and each family’s the result of one or more exogenous infections by a particular virus or family of viruses. If that virus is only common in part of a species’ range (because its vectors or carriers live there, or because that’s where the species’ Patient Zero happened to be, or whatever,) then couldn’t the ERV family be initially confined to that area?

    If our common ancestor had a geographical distribution of ERV families, and speciated allopatrically, then descendant species might end up inheriting different families.

    But as you say, this obviously couldn’t be the case for an ERV family if it really had arisen over ten million years beforehand!

    And particularly CERV 2 is way too old to have been maintained as an ancestral polymorphism up to the chimp-human split.

    Only if the age estimate the authors compute via sequence divergence is correct, and they themselves apparently doubt that, writing that the estimate is “inconsistent” with other facts they provide. In the two other cases of anomalously old ERV families–CERV 1 and CERV 3–they explain why sequence divergence might skew the age estimate high, and I think the same considerations are supposed to apply to CERV 2. (Their discussion of CERV 2 is, explicitly, largely a repeat of the bit on CERV 1.)

    But I think the authors are not referring to ancestral polymorphisms, but indels and new insertions after the human-chimp(s) split, to explain the differences.

    They rule out deletions entirely, though, writing, “Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.”

    I think the authors’ main explanation is that their age estimates are simply wrong here. Either these families are the result of insertions entirely after the human/chimp split, as you suggest, or they’re (slightly) older than the split and weren’t yet fixed when it occurred.

  92. #92 Anton Mates
    April 19, 2009

    cprss,

    Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term ‘orthologues’ is presumptive only,

    But this paper (the PLoS one) does not claim that any of the insertion sites it covers are orthologous. It claims that 24 out of 299 are ambiguous, and that the other 275 are not orthologous. The latter claim doesn’t presume anything; you don’t need to precisely localize two insertion sites to confirm that they’re not in the same place.

    and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved – the argument cuts two ways.

    Is there a reason it should confirm any such thing? This (the paper mentioning 42 families of chimp ERVs) was, well, a paper surveying chimp ERVs; it wasn’t trying to establish anything about primate phylogeny.

  93. #93 windy
    April 19, 2009

    Anton:

    They rule out deletions entirely, though, writing, “Again, we were able to detect pre-integration sites at those regions in the human genome orthologous to the CERV 2 insertion sites in chimpanzees, effectively eliminating the possibility that the elements were once present in humans but subsequently excised.”

    For CERV 2, but the paper identifies several instances (Table 3,4 & Figure 6) in other families where the retrovirus was excised (leaving LTRs) or the whole region was deleted (no intact pre-integration site to explain).

    cprs:

    Fair enough, but where precise sequencing does not confirm the insertion site, there are two important corollaries, strictly the use of the term ‘orthologues’ is presumptive only, and without further study none of the data from the 42 families of CERVs in this particular paper yet confirm monophyletic descent for any of the primates involved

    Err whut? They say they DID identify orthologues in all but two of the families. Just to see that they weren’t kidding about the orthologues, I picked one of the ERVs from Table 2:

    CERV 5 (HERV15) 20:22151622..22161290

    The coordinates refer to the Ensembl genome browser, so this should be the view of the position of the ERV in the chimp genome.

    I downloaded the sequence of “Contig71.30″, which is a sequence assembly of the region, about 60,000 bp, which encompasses the ERV’s ~9,700 bp. When I do a BLAST search of this contig against the human genome, it’s a 99% match, so it would appear that the ERV is in the same place there (otherwise it would show a gap!)

  94. #94 Shrunk
    April 19, 2009

    It’s not actually clear to me that when they use the term “orthologous” this necessarily means that the ERV’s are located at the same site in the genomes of both species. It seems to me they are simply using it to refer to ERV’s that have resulted from the same virus. Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

  95. #95 Anton Mates
    April 19, 2009

    windy,

    For CERV 2, but the paper identifies several instances (Table 3,4 & Figure 6) in other families where the retrovirus was excised (leaving LTRs) or the whole region was deleted (no intact pre-integration site to explain).

    That’s quite true. It’s only certain subfamilies in CERVs 1 and 2, and that single CERV 3 element, for which the inconsistency arose (no human orthologues, no apparent deletion, and clocked by their age estimator as older than the chimp-human split.)

    Shrunk,

    Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

    That’s not too surprising, though. The vast bulk of chimp ERVs were unknown before this study, so no previous paper would have found anywhere near as many common insertion sites. Even nine of the human ERV families found to be orthologous were first identified in this study. (See the associated letter at http://jvi.asm.org/cgi/content/full/80/9/4640?view=long&pmid=16611924#T1 .)

  96. #96 windy
    April 19, 2009

    Otherwise, that would mean that there are at least 40 identical ERV insertions between humans and chimps, which is much higher than any figure I have heard elsewhere.

    If there are tens of thousands of ERVs in the human genome, it’s hardly likely that most of them would have been inserted after the chimp-human split! If we in fact had less than 40 shared insertions, I’d say that would falsify chimps and humans as sister species…*

    *just to be clear for Willy’s and cprs’s sake, this is a counterfactual scenario, we share more insertions than that. The paper identifies three types of ERV families: families where no new insertions have occurred after the chimp-human split, families which have orthologues *and* some new insertions in either of the species (indicating that the ERV has been active both before and after speciation), and families which occur only in chimpanzees. As we would expect if the species have recent common ancestry, the non-shared families are a minority.

  97. #97 Shrunk
    April 19, 2009

    If there are tens of thousands of ERVs in the human genome, it’s hardly likely that most of them would have been inserted after the chimp-human split!

    Is that true, though (Honest question, not rhetorical)? Of course, we would expect more ERV’s to have been inserted into our genome prior to the divergence with chimpanzees. But since these are nonfunctional genes, and therefore not conserved by selective pressure, how many of these would survive to the present day? It could be argued that more recent ERV’s (i.e. those inserted after divergence from chimps) would predominate in our genome, having had less time to be degraded by mutations. Otherwise, we could also expect to find the genome to be abounding in ERV’s shared with all other organisms with whom we share a common ancestor, which of course is all organisms, period (limited by the fact, of course, that not all organisms develop ERV’s). If that were the case, I would expect ERV’s to make up an even greater percentage of our genome.

    But I could be wrong, and welcome more informed opinions.

  98. #98 windy
    April 19, 2009

    Is that true, though (Honest question, not rhetorical)? Of course, we would expect more ERV’s to have been inserted into our genome prior to the divergence with chimpanzees. But since these are nonfunctional genes, and therefore not conserved by selective pressure, how many of these would survive to the present day?

    Of course they are degraded over time, but that doesn’t mean that they are lost that fast. From Wikipedia on ERVs:

    There are many thousands of endogenous retroviruses within human DNA (HERVs comprise nearly 8% of the human genome, with 98,000 elements and fragments[7]). All appear to be defective, containing nonsense mutations or major deletions, and cannot produce infectious virus particles. This is because most are just long-lasting traces of the original virus, having first integrated many millions of years ago. However, there is one family of viruses that have been active since the divergence of humans and chimpanzees.

    Otherwise, we could also expect to find the genome to be abounding in ERV’s shared with all other organisms with whom we share a common ancestor, which of course is all organisms, period

    You are making a false dichotomy here. You assume that either almost all ERVs older than the human-chimp ancestor should have been completely lost, or that you should be able to find ERVs from ALL of our ancestors no matter how old. Of course, the truth is somewhere in between. There are a lot of other non-coding loci that are shared between humans and some or all other primates, like pseudogenes and microsatellites, but none that are shared with all organisms.

  99. #99 cprs
    April 22, 2009

    Thanks to all, but esp to Windy, most interesting to see the raw data and how easily obtained it is with a good guide – indisputably highly homologous regions without gaps – and I can understand well founded the claim of orthologous sites is for CERV5 for example.

    Given criteria as rigorous, the orthologous CERV 1 and 2 sites for man and orangutan are all indisputably missing without trace, and these for viruses with subfamilies of estimated ages of 5, 7.8, 14 and 21 Mya.

    Anton ‘Shrunk’s suggestion, which []he says is based on correspondence with the authors, is that they simply never went to fixation in the human-chimp common ancestor in the first place. ‘

    If ERVs inserted in the germline of common ancestors how have all the traces of all of these disappeared?

    Windy ‘just to be clear for Willy’s and cprs’s sake, this is a counterfactual scenario, we share more insertions than that. The paper identifies three types of ERV families: families where no new insertions have occurred after the chimp-human split, families which have orthologues *and* some new insertions in either of the species (indicating that the ERV has been active both before and after speciation), and families which occur only in chimpanzees. As we would expect if the species have recent common ancestry, the non-shared families are a minority.’

    The nonshared families are numerically large and reportedly contain numerous orthologous sites in other species (>100 CERV1, most heterologous and ?14 CERV2, based on fig.4′s LTR tree http://genomebiology.com/2006/7/6/R51/figure/F4). Do you confidently attribute all this loss to lineage sorting/genetic drift?

    This thread’s ageing now – but I welcome critical comments.

  100. #100 Shrunk
    April 22, 2009

    It seems to me that the only problematic part of the evidence is the estimated age of the ERV’s. Otherwise, the observed data is easily explained by independent insertions into the various lines after divergence. As I’ve said, I don’t have any expertise in this area; I don’t know if the explanation is as simple as that the estimated ages are just wrong.