Biology Evolution Intelligent Design

Endogenous Retroviruses in the Case for Common Ancestry

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We often hear the argument that evidence for common ancestry can also be interpreted as evidence of common design. Some years ago I made the argument that there was no way to discriminate between the two. The argument was countered (successfully IMO) by endogenous retroviruses (ERVs).

A bit of background about ERVs. Retroviruses replicate themselves by invading a host cell and inserting a package of viral genes into the host DNA along with promoters that cause the cell to express (translate and manufacture into proteins) those genes. The expression of those genes makes new virus particles and can compromise or kill the host cell in the process. The active viral gene package, after insertion, is called a provirus. Proviruses can be deactivated by a number of means becoming inert and leaving just the mostly intact but non-functional genes still in the host cell genome. Occasionally a germ cell can become infected and if it survives to become a new organism the deactivated provirus becomes what’s called an endogenous retrovirus (ERV for short) and gets passed along from parent to offspring down the lineage. Because the ERV serves no function it is not conserved by natural selection and is slowly mutilated by random mutations over millions of years until it is no longer recognizable as the strain of provirus it once was. There may be preferred insertion points in the genome for the RV genes but if there are there are a great many potential insertion points.

The case for common ancestry is made by finding the same strain of ERV inserted at the same place (loci) in the genomes of closely related species such as different primate species. The argument is that the RV infected a germ cell in a common ancestor and the ERV was then inherited by all the descendents. When the species splits or spawns a new species that is reproductively isolated each species has the ERV but, and here’s the key, random mutation changes each ERV differently. By comparing the differences in ERV sequences at the same loci in different species one can establish a rough date for the original infection in a common ancestor given a more or less average background rate of random mutation.

ERVs in various levels of decomposition make up some 8% of the human genome. Occasionally however an ERV is conscripted for some useful purpose and is conserved. It should be noted that human designers use domesticated RVs as delivery vehicles to insert foreign genes into genomes to create so-called GM (genetically modified) organisms like tomatoes with longer shelf lives and whatnot. Theoretically this can be used to distribute vaccines for various diseases. A GM banana for instance could carry genes that cause it to manufacture a vaccine for malaria. Eat a GM banana and you’re immunized against malaria. More significant to the case for intelligent design is that this is a mechanism a designer could use to modify genomes – introduce a virus into the population which inserts genes that cause the spawning of a new species. So if anyone asks about possible mechanisms a hypothetical designer could use to intervene and direct evolution that’s a good answer. Human designers are already doing it so it’s a proven mechanism. Morever a highly infectious retrovirus inserting genes that cause modification and speciation could convert entire populations into a new species in just one or several generations and at the same time cause the original species to become extinct virtually overnight. That fits wonderfully with the indisputable testimony of the fossil record which paints a picture of abrupt speciation, millions of years of little if any change in the new species, followed by an abrupt extinction. A mechanism for causing saltation of new species is thus shown.

Anyhow, back to the case for common ancestry. Recently in a private forum where others are concerned with intelligent design I brought up the case of ERVs as evidence supporting common ancestry vs. common design. If common design instead of common ancestry the designer is evidently using existing species in situ as the template for new species. If that’s the case there’s effectively no difference whatsoever between common design and common ancestry.

An objection was raised about how it was possible for a germ cell to become infected by an RV in the first place and secondly how could it survive the infection and go on to grow into a reproducing adult. As it turns out it probably isn’t very likely at all for sperm cells to be either infected with a provirus or survive the infection. Sperm are created and grow quickly into mature cells with a lifetime measured in days. Once mature they are stored behind a blood barrier which inhibits viral infection. They are also very active cells and even if infected would likely be hobbled enough to not be successful at fertilizing an egg. Egg cells however are a whole different story. In mammals a female is born with a lifetime supply of primary oocytes (immature egg cells) already created. There is also no blood barrier where they are stored in ovarian follicles. They are stored in a state of suspended animation or dormancy. Upon their creation in the developing embryo meiosis is halted in the first of two meiotic divisions at anaphase (IIRC) while still diploid (full compliment of 46 chromosomes). DNA replication and segregation into haploid germ cells is not completed until, beginning with puberty, one or a few resume meiosis and become mature egg cells ready to be fertilized. Thus a primary oocyte can hang around in a dormant state for 50 or more years and ostensibly be infected by an RV at any time. Because they are dormant gene expression is suppressed and even after a provirus is inserted into their DNA it isn’t likely to be expressed. The provirus remains dormant as well in other words. Because meoisis hasn’t progressed very far there is still a lot of DNA replication and shuffling (segregation and crossover) that goes on before the egg is mature. My conjecture is that the provirus is deactivated or very likely to be deactivated during the completion of meiosis (possibly from either segregation or crossover) so it is converted at once from provirus to endogenous retrovirus without ever having an opportunity to be expressed into new virus particles. This would handily explain how so many ERVs have found their way into primate genomes.

116 Replies to “Endogenous Retroviruses in the Case for Common Ancestry

  1. 1
    Atom says:

    Hey Dave, thanks for this post and the info on ERVs.

    I have a question (forgive me if this betrays ignorance on my part). Let’s say an organism gets infected, and thus gets this new gene. We can think of it as a new “allele”. What causes this new allele to become fixed in the population so that every member of the species eventually has the same gene?

    Does it provide a selection value to take over a population?

    If not, then won’t random effects cause the one copy of the gene (from the infected organism) to probably not become fixed?

    The way I see it, there are two chance events: 1) the egg cell becoming infected (don’t know the odds here, but they would be relevant), and 2) the new gene becoming fixed in the population (we have a rough estimate on this).

    Am I looking at this the wrong way? To me it would seem that any claim that a copy of a gene spread to all members of a population has the same difficulties whether we’re dealing with a random-mutation caused gene or a virally inserted gene.

  2. 2
    Atom says:

    PS Sorry if I was loose in my terminology, interchanging “gene” and “allele”…I understand the difference. I think my post is sufficiently clear on what I meant, but I’m sorry for being sloppy in that regard.

  3. 3
    bornagain77 says:

    Dave,
    I’m still not buying the reasoning that the viruses were somehow responsible for totally new species. The novel information required for jumps between species is measured in millions of base pairs of DNA. I don’t know how much information a virus can insert into DNA at one time, but I believe whatever information it inserts is sequential in nature. I think the problems of your scenario are obvious because of the required numerous specific and beneficial modifications that have to be made in different regions of the genome, not to mention the changes that have to be made to the cell itself. Unless a virus can make specific modifications to many different sites without embedding itself into the DNA, and then disappearing and leaving no trace in the cell. Your scenario is unconvincing at first glance.
    I also remind you that is still “Just” an educated guess on the evolutionists part that says the information of the ERV is an inherited characteristic of a common ancestor.
    Indeed we are still mearly infants in our understanding of the Genome. The Genome is so complex man may never be able to fully decipher it. I think it is very premature to put stock in anything the evolutionists have to say about how information got into the genome… VERY PREMATURE INDEED!!

  4. 4
    scordova says:

    Even as someone who rejects common ancestry, I readily concede the arguments for common ancestry are formidable.

    I would like to point my creationist brethren to an excellent article by creationist biologist Dr. Todd Wood who highlights the arguments in favor of common ancestry.

    He and I do not accept common ancestry, however, we both recognize common ancestry is not an unreasonable position (unlike unreasonable positions such as a belief in mindles OOL).

    The Chimpanzee Genome and the Problem of Biological Similarity

    Wood offers the difficulty creationists face:

    THE FUTURE OF CREATIONIST GENOMICS

    The genome revolution, exciting though it is, is not an obvious victory for creationism. Although more data allows for better testing of ideas, the data that we have present significant challenges to creationist theory, particularly in the realm of biological similarity. I am confident that a solution to most of the problems in this article will be forthcoming. How quickly these issues are resolved, however, will depend entirely on our research priorities and how we choose to pursue those priorities. If we wish to be good stewards of our very limited resources, we should avoid projects that are unlikely to be productive (e.g. overemphasizing potentially insignificant differences or trivializing the striking similarities) and focus instead on one of the most pressing problems in biology, biological similarity.

  5. 5
    bornagain77 says:

    Similarities is evolutionists strongest point of contention, yet you forget a few things. Scientists are to the point of declaring ALL mutations to DNA detrimental to the organism. This keeps in line with the second law of thermodynamics. As well The seemingly beneficial mutations, which still keep in line with the entropy of information by the way, are on the verge of being declared “calculated” mutations. This will prove a higher level of design in the cell and further alienate the evolutionists fallacy.
    I’m not scared of the similarities at all. The virus myth is just another blind alley for evolutionists. Hopefully breakthroughs will be forthcoming that will reveal purpose for the “virus” information.
    As a sidelight to this, I find the fact that viruses allow communication to the enviroment for populations of bacteria to be interesting to our topic. Could it be some comunicative type code that allows cells to “talk” to each other.
    I know it is just a guess, but when you really think about it, that is all evolutionists are really doing with the similarities anyway! They totally ignore all other lines of evidence that doesn’t support there narrow view. I also remind you that evolutionists have always severely underestimated the level of complexity that they are dealing with.

  6. 6

    In that thread, I pointed to a study which a virus appeared in mice as well as humans(?). Maybe someone could find the link in the comments.

    I did find this: http://www.pnas.org/cgi/conten.....03836103v1

    So retrovirus’s could have design characteristics.

  7. 7
    pk4_paul says:

    Atom raises a very good point:

    I have a question (forgive me if this betrays ignorance on my part). Let’s say an organism gets infected, and thus gets this new gene. We can think of it as a new “allele”. What causes this new allele to become fixed in the population so that every member of the species eventually has the same gene?

    Does it provide a selection value to take over a population?

    If not, then won’t random effects cause the one copy of the gene (from the infected organism) to probably not become fixed?

    Why should a genomic change become fixed in a population unless it provides a benefit to an organism? Even if a benefit can be described we cannot be certain of it spreading throughout the population. All primate populations carry a genetic load. More to the point, when two recessive alleles are present and the related phenotypic trait is expressed reproductive fitness is in no way perceptibly lessened by it when its effects are slight. All of us carry some slight genetic defects that explain some of our physical traits. This post is an interesting one, as is the analysis contained in it, but until Atom’s question is resolved it appears that those touting retroviral evidence for common descent need to explain how the allged events are consistent with their depiction of natural selection’s role in evolution.

  8. 8
    DaveScot says:

    atom & pk4_paul

    What causes this new allele to become fixed in the population so that every member of the species eventually has the same gene?

    A significant fraction of the population getting infected by the same retrovirus over a small number of generations would be my guess. If mortality rate is low, tranmission rate is high, and germ cell infection is common it could become fixed in a single generation. I’m a little surprised no one thought about the difference between a viral gene and a new allele. Viruses spread horizontally and with great rapidity through a population. The same gene finding its way into many individuals or even an entire population requires no reproduction of the host at all. A single sneeze can put the viral genes into everyone in your cave all at once. Alleles can’t spread that way – unless of course they happen to get picked up as an accidental tourist by a retrovirus which is also well within the realm of physical possibility. Horizontal gene flow via prophages and plasmids is common in prokaryotes, at least significant in protists, and at least suspected of being significant in complex multicellular organisms.

    ba77

    I’m still not buying the reasoning that the viruses were somehow responsible for totally new species. The novel information required for jumps between species is measured in millions of base pairs of DNA.

    I must have missed the research that determined how many genetic modifications were required to change one primate into another. I was under the impression that all we know is how many differences there are and we have no clue how many of them are actually required. I do know that modification of a single existing gene, or just the regulatory region for a gene that causes more or less of the protein to be manufactured at different times, has been shown to cause cascade effects throughout the entire organism in totally unexpected ways. A quick look around for number of base pairs in a retrovirus found a couple of hits in the neighborhood of 10,000. The theoretical upper limit is something I didn’t see (but I didn’t look very hard). Keep in mind genes can do really weird things like make copies of itself all over the place (retrotransposons). The copies can have different effects depending on where they land. There’s no reason to presume a designer would be limited to one virus nor does any single virus have to have an immediate effect. A long series of ERVs that lie dormant until a final one activates the whole lot into action is possible. This is so speculative (but quite possible) the best reading I can recommend on speciation via ERV mobilization is Greg Bear’s highly acclaimed hard science fiction book “Darwin’s Radio”. Read this article I wrote http://www.uncommondescent.com.....evolution/ in January that mentions Darwin’s Radio and links to a review of it published in Nature.

  9. 9
    Bob O'H says:

    Let’s say an organism gets infected, and thus gets this new gene. We can think of it as a new “allele”. What causes this new allele to become fixed in the population so that every member of the species eventually has the same gene?

    Does it provide a selection value to take over a population?

    If not, then won’t random effects cause the one copy of the gene (from the infected organism) to probably not become fixed?

    Yes, you’re right. If a new allele is neutral, then it probably won’t become fixed. However, a lot of new alleles are being produced over time, so even if most disappear, a few will become fixed.

    Fixation can be facilitated by a small population size, and in particular things like population crashes, or migration into a new area by a small number of individuals can have a large effect on fixation.

    So, a selective advantage isn’t necessary for fixation, but it does help!

    Bob

  10. 10
    bornagain77 says:

    Thank You Geoff Robinson,
    To refute the Evolutionists ERV scenario it is necessary to find deeper purpose for the ERV information in the genome. at this site which Mr. Robinson points to in his post;
    http://www.pnas.org/cgi/conten…..03836103v1

    I found this statement:

    This work supports the hypothesis that ERVs play fundamental roles in placental morphogenesis and mammalian reproduction.

    So the ERV code does have specific purpose communicating between the cells. This is Much like the communication viruses enable in the bacterial community.

    According to evolutionary Dogma the majority of ERV in the genome have no function. Yet when tested for function they are shown to have specific function in the development of fetuses.

    As I stated before, Evolutionists have always blatantly underestimated the complexity they are dealing with in the genome. From their terrrible track record in the past we are justified to remain highly sceptical of anything the evolutionists choose to say about the information in the Genome.

  11. 11
    Joseph says:

    I disagree with Sal (apologies) in that the evidence for common ancestry is very weak. I say that because we still don’t have any data which demonstrates what caused (causes) the physiological and anatomical differences observed between allegedly closely related populations- like chimps and humans.

    To this day we don’t even know if such a transformation is even possible.

    But anyway- ERVs:

    In order for an ERV to be in the same location in differing populations via Common Descent, either many individuals in the originally infected had to be infected at the same locus or there was a survivable bottle-neck. IOW only one got infected and that one passed on the genetic material that all subsequent populations received.

    And if multiple individuals got infected at the same locus/ loci then that would mean a common mechanism is at play.

    Next comes meiosis with its chromosomal recombinations being the norm. So not only does the ERV have to survive that bottle-neck it has to stay in place all the while rearrangements are taking place all around it.

    And in the end it could be that these sequences just look like ERVs- convergence could explain that. They also could be part of a common design that we just don’t understand- yet. (one common design scenario could be that these are ERV decoys that won’t allow new viral insertions)

  12. 12
    Atom says:

    DS,

    “Viruses spread horizontally and with great rapidity through a population. The same gene finding its way into many individuals or even an entire population requires no reproduction of the host at all.”

    This reminds me of Spetner’s hypothesis of species-wide spontaneous mutations in response to environmental queues. A similar pattern of spreading is seen.

    But back to ERVs. Indeed, a viral event would have to overtake a majority of the population each time we find one of these, injecting itself into gametic cells, not harming the reproductive aspects of the host, then remain in the genome without being removed by random effects and recombination, happening several times in different species.

    I don’t know the probability of your scenario for species-wide gametic infection, but unless you have independent evidence that this most likely happened, it would seem that the ERV case isn’t super strong. Your scenario indeed removes the burden of a single new gene having to spread throughout the population, but it itself seems like it may require more than one unlikely event.

    So at the moment, I’d say it is better to be cautious when using ERVs as evidence of anything, since we are just beginning to understand their function and guess at their history.

  13. 13
    mike1962 says:

    scordova, “Even as someone who rejects common ancestry, I readily concede the arguments for common ancestry are formidable.”

    Just curious, but why do you reject common ancestry if the arguments for it are formidable?

  14. 14
    bFast says:

    bornagain77:

    I’m still not buying the reasoning that the viruses were somehow responsible for totally new species.

    I don’t see ERVs as playing any significant role at all in the development of new species, ERVs are a marker. However, there are only two explanations I can find for why chimps and humans would have this same virus-caused marker. The first is that the marker landed in the genome of the common ancestor prior to the chimp/human split. The other expanation is that the designer intentionally placed the marker in his new human creation. Why did he do that? Two possible explanations, the DNA that we see as the product of ERVs plays a valuable role in the DNA of the human, or the designer did so in order to make a unique creation appear to be the product of common ancestry. Ie, he’s foolin’ us — lying.

    Again the options are:
    1 – ERVs prove that humans and chimps had a common ancestor or
    2 – The desiger (God) put the ERV code into a special creation because:
    2a – It actually plays a meaningful role or
    2b – God specially created humans to appear as if we have a common ancestor. Ie: he’s just foolin’ — lying.

    As 2b is anathema, either 1 or 2a must be the case. My vote, my very strong vote based up on the evidence is for common ancestry. That said, I am not so convinced that all of life stemmed from a single common ancestor. It is well reasonable that there were three, one for each domain. However, the cambrian explosion may also have been a special creation event. Were the reptiles a special creation event? Mammals? It seems rather likely to me that all mammals share a common ancestor.

  15. 15
    bornagain77 says:

    Mike 1962,

    All the “Suggestive evidence” you allude too, but do not name specifically, for common ancestry (my guess is similarities of some type), has a irreconcilable flaw with reality. You have no method or process whatsoever to account for the generation of meaningful information in the genome, as the following quotes illustrate.

    “But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.” Lee Spetner (Ph.D. Physics – MIT)

    “There is no known law of nature, no known process and no known sequence of events which can cause information to originate by itself in matter.” Werner Gitt, “In the Beginning was Information”, 1997, p. 106. (Dr. Gitt was the Director at the German Federal Institute of Physics and Technology)

    You base your conclusions on faulty suggestive evidence that has no basis in the evidence we have established for the integrity of the DNA.

    Theism postulates that the DNA of man is complete and ANY mutations to it will be detrimental in some nature, This is exactly what the evidence of exhaustive experimentation is pointing too. Evolution is left wanting for a mechanism of novelty and all presumptions to arise from the evolutionary scenario are meaningless until evolutionists can clearly demonstrate a gain in genetic information that would violate the entropy of information!
    This is not some minor point I point out, this one point is the very crux of the battle between ID and evolution!

  16. 16
    Smidlee says:

    IF you are very selective in your evidence then yes some have made a good case for common ancestor. But in my view it totally falls apart when you look at the overall big picture. This is the same with fossils, they really don’t support common ancestor unless you are very selective (sometime to the extreme) in what is considered evidence. To me not very convincing.

  17. 17

    DaveScot wrote:

    “. . . this is a mechanism a designer could use to modify genomes – introduce a virus into the population which inserts genes that cause the spawning of a new species . . .”

    Let’s see, a virus “inserts genes.” Which genes and what do they do? Can they really “cause the spawning of a new species?” What about epigenetic information, which is increasingly understood to be significant and extensive — all the way from the cellular structure to the level of organs and the entire organism. Seems like we are talking about another just-so story at this stage, based on the inaccurate, or at least incomplete, central dogma that information travels in only one direction from the DNA.

    The problem of getting information into the DNA is of course horrendous (from a naturalistic perspective). Yet it is hardly the only problem to be overcome in getting from one species to the next. Might it be sufficient to account for all the differences between species within a single genus? Questionable, but possible. Does it account for all the differences at higher levels? Exceedingly unlikely.

    An interesting topic worthy of further consideration, to be sure, but not terribly convincing as of yet.

  18. 18
    Jehu says:

    Again the options are:
    1 – ERVs prove that humans and chimps had a common ancestor or
    2 – The desiger (God) put the ERV code into a special creation because:
    2a – It actually plays a meaningful role or
    2b – God specially created humans to appear as if we have a common ancestor. Ie: he’s just foolin’ — lying

    Or the virus inserted itself at the same loci in different species.

  19. 19

    bornagain77 wrote:

    “Theism postulates that the DNA of man is complete and ANY mutations to it will be detrimental in some nature, This is exactly what the evidence of exhaustive experimentation is pointing too.”

    I’m not sure which theism this would be. I doubt this is the position of most official mainstream religious views.

    You do have an excellent point, however, that the great weight of the evidence points toward a system well designed from the outset, and with respect to which deviations are generally detrimental.

    One can, of course, scour the landscape of biology and come up with a handful of examples of (i) on the one hand, “poor” function or design, and (ii) on the other hand, deviations/mutations that are helpful in some limited sense to the organism. We ought to frankly acknowledge these observations when they are made, but we ought also to see them in the broader biological context — which context clearly demonstrates that such examples are the very exceptions that prove the rule.

  20. 20
    pk4_paul says:

    Dave Scot wrote:

    A significant fraction of the population getting infected by the same retrovirus over a small number of generations would be my guess.

    If this were the case one would not expect to see insertion points at identical locci if this were truly a random process. But I am aware that there is excellent evidence for preferential insertion points. The significance of this lies in the use of ERVs by Darwinists to argue for common descent. If insertion points occur at preferred locations and a retroviral outbreak occurs, one would expect to see the evidence for this not only in the same genomic locations within a species, but also perhaps for different species, as would be the case for primates who have very similar genomes. Identical preferred insertion points would explain the presence of ERVs at the same locations in two species having very similar genomes. This still would not explain why genomic junk would be preserved over geologic time periods and indicates a natural selection anomaly.

    If mortality rate is low, tranmission rate is high, and germ cell infection is common it could become fixed in a single generation. I’m a little surprised no one thought about the difference between a viral gene and a new allele. Viruses spread horizontally and with great rapidity through a population. The same gene finding its way into many individuals or even an entire population requires no reproduction of the host at all.

    This is fascinating to contemplate. However retroviruses leave a genomic signature behind by which they are identifed. In addition for an ERV to become a functional part of a eukaryotic genome we would expect to find promotor regions, an initiation site and required transcription factors enabling gene expression.

    I’m not a believer in accidental causality and before one invokes selection to explain how an accident becomes deterministic I’d like a clearer indication that selection is not an ad hoc concept, that can explain both the retention of junk over geologic time, as well as slightly beneficial theoretical changes.

    A related interesting question lies in accounting for the origin of viruses themselves. From a Darwinian perspective they are problematic being host dependent.

  21. 21
    bFast says:

    Jehu, “Or the virus inserted itself at the same loci in different species.”

    This is a nice hypothetical solution. It would seem to hold merit if there were some cause why the ERV was inserted at that particular location, and would hold merit if there were very few such events. However, not only do ERVs show this phenomenon, but as discussed on Brainstorms recently, there are also around a hundred defined disease producing point mutations that are common between the human and the chimp. The evidence suggests that humans and chimps have a common ancestor. The best reason I can find to conclude that that is not so is a religious conviction. I, for one, do not want science bridled by religious conviction whether that be the conviction that some text is divine, or the conviction that there is no divine. Let the evidence speak for itself.

  22. 22

    bFast wrote:

    “Let the evidence speak for itself.”

    Absolutely agree. We should be willing to let that evidence challenge our personal religious and philosophical convictions.

    “. . . there are also around a hundred defined disease producing point mutations that are common between the human and the chimp.”

    Ah, yes, but how many are there that are different? Further, is there an explanation for the similarities that does not rely on common descent? To use a crude example, how many common points of failure exist between a car and a 747? Probably several dozen at least. Does that mean they descended from each other?

    I have no particular philosophical issue with the idea of common descent. I am, however, skeptical of looking at a set of existing comparisons and assuming that this gives a historical narrative. Comparative genomics is a useful exercise, but it is, in principle, an undertaking eerily similar to comparative anatomy. One may find comparative genomics more compelling, but the undertaking is the same. I can easily come up with several dozen similarities between a lion and an elephant. Does that mean one is descended from the other? Comparative analyses are interesting, but they must be kept in context, and their inherent and significant limitations must be respected.

    I have no issue with common descent. Nevertheless, I remain highly skeptical, based on my, admittedly limited, review of the evidence that is cited. Similarities between species are noteworthy and interesting. It is also interesting to think about how similarities might be preserved from one species to the next. Yet what is conspicuous by its very absence is any compelling mechanism that can explain the origin of the differences.

  23. 23

    I found my old comment. I’ll reproduce the comment since I forget the details:

    There is an instance of convergence of retroviral sequences which perform the same function between mice and primates. Since there isn’t common ancestary between those two, that retroviral instance would lend us more towards design.

    http://www.pnas.org/cgi/conten.....06509102v1

  24. 24

    “There is an instance of convergence of retroviral sequences which perform the same function between mice and primates.”

    Oh, that’s just great. Now we’re back to explaining these with our old standby, ad-hoc explanation of convergent evolution?

    So it is evidence for a common relationship . . . except when it is not . . .

    Forgive my skepticism.

  25. 25
    Mung says:

    [quote]Your scenario indeed removes the burden of a single new gene having to spread throughout the population…[/quote]

    An unnecessary concession. DS stated talking apples and oranges. Go back and examine the originally porposed scenario, and the problem persists.

    [quote]2b – God specially created humans to appear as if we have a common ancestor. Ie: he’s just foolin’ — lying.[/quote]

    This fails as an argument against design, for obvious reasons.

  26. 26
    bornagain77 says:

    Bfast wrote,
    there are also around a hundred defined disease producing point mutations that are common between the human and the chimp. The evidence suggests that humans and chimps have a common ancestor.

    Now this is extremely interesting, you claim common ancestor from similarities. Yet you have no knowledge as to what actually caused the mutations (could it be some type of calculated response of the genome to stress).
    Yet despite mountains of evidence indicating that information cannot be generated in the genome by natural means you claim proof of evolution because of similarity of the genome, and ignore the fact that you have no mechanism for generating information in the genome in the first place, You should instead be looking for a more probable cause for the similarities. (My guess, is that they are not random mutations at all but most likely are “calculated” mutations to stress from some type of prexisting biological feedback loop that scientists have not yet fully defined.)

  27. 27
    pk4_paul says:

    bFast:
    This is a nice hypothetical solution. It would seem to hold merit if there were some cause why the ERV was inserted at that particular location, and would hold merit if there were very few such events. However, not only do ERVs show this phenomenon, but as discussed on Brainstorms recently, there are also around a hundred defined disease producing point mutations that are common between the human and the chimp.

    The nice hypothetical solution has solid empirical support and there are also biochemically based explanations, related to mutations, that explain probability based on the nature of certain mutagens and how DNA repair mechanisms function. It is helpful to review the history of this issue because it illustrates which side is seeking the “nice solutions.” When common descent arguments were advanced based on genomic evidence of viral insertions Darwinists made the unwarrented assumption that such insertions were random. The advantages to such a claim were obvious. They also bear a suspicious witness to an ideological bent. But what happens when subsequent studies reveal that insertion points are not random. In most scientific fields the reversal of a claim would cast suspicion on the theory it was used to support. But what do we have here. Is the notion of common descent compromised? By no means. An adjustment is made and it is now claimed that common descent accounts for the genomic features that determine preferred insertion points. Heads I win. Tails I win too.

    The evidence suggests that humans and chimps have a common ancestor. The best reason I can find to conclude that that is not so is a religious conviction. I, for one, do not want science bridled by religious conviction whether that be the conviction that some text is divine, or the conviction that there is no divine. Let the evidence speak for itself.

    I have a different perspective on this. It seems to me that science is better served when layers of causality are minimized. The relevant data explaining why a retrovirus would be inserted at such and such a location are connected to biochemical causes. When we find out the details we are able to explain problems. Common descent is not a helpful concept in solving these kinds of problems. This is a case study as to why this is so. Common ancestry is layered on to actual explanations and if there are two alternatives, x and y, both can be incorporated into a common ancestry paradigm by making the necessary adjustments. Common ancestry is never threatened. It is an endlessly flexible doctrine. Ironically those with religious views are frequently accused of blind adherence to dogma by those hostile to religion. Yet can any theory linked to science be any more dogmatic than common descent? Believe that which you will. If common descent explains everything then its real utility is virtually nil.

  28. 28
    Fross says:

    Hey geoffrobinson, how’s it going?

    So here’s the thing with ERV’s and how they are seen as evidence for common descent. They actually have to meet two criteria to be seen as evidence for common descent. 1. same location on DNA 2. sequence patterns have to be consistent.

    This is practically the same methods they use to determine paternity tests on humans.

    The study you linked to above was not discussing ERV’s in this manner. For one, they weren’t found in the same DNA locations between humans and mice and they didn’t have the same sequence. They were only similar in function.

    I hope this helps.

    later man, and have a good weekend.

  29. 29
    Atom says:

    [quote]Your scenario indeed removes the burden of a single new gene having to spread throughout the population…[/quote]

    An unnecessary concession. DS stated talking apples and oranges. Go back and examine the originally porposed scenario, and the problem persists.

    I guess I should be more specific:

    Dave’s virus-hits-every-member-of-population scenario indeed removes the burden of a single new gene in one organism having to takeover the population by reproduction and selection (thus bypassing Haldane-ReMine limits and random effects)…

    Atom

    PS Mung, BBCode doesn’t work on these boards. Use <blockquote></blockquote> tags instead to offset quotes.

    ex <blockquote>Text to offset goes in here</blockquote>

  30. 30
    bFast says:

    geoffrobinson #23, you provide an interesting post. This data would, in fact, support DaveScot’s assertion that a designer may use ERVs as vehicles to inject functional DNA into organisms. (Believe me, just because I buy into common ancestry, that doesn’t mean I reject agency.) However, as was pointed out, this is an example of a similar ERV in two separate lines, but at very different locations in the genome — hardly a viable argument against the proof of common ancestry sited. (according to common ancestry theory, they do have a common ancestor, by the way, just not in the last 20m years when the ERV apparently was injected.)

  31. 31
    mike1962 says:

    bornagain77,

    Not sure what my question to Salvador has to do with your post to me. Common ancestry has no necessarily logical connection with random mutation providing new information. One can accept common ancestry and reject RM+NS as the engine of that ancestry.

  32. 32
    mike1962 says:

    bFast, “2b – God specially created humans to appear as if we have a common ancestor. Ie: he’s just foolin’ — lying.”

    2c: After the fall of man, God allowed Satan to mess with the creation and put all kinds of deceiving evidence in there. This idea is quite compatible with Christian theology. The New Testament speaks of “lying wonders” and a “great delusion” God allows Satan to pull off prior to the Second Advent, etc.

  33. 33
    Mung says:

    I guess I should be more specific:

    Dave’s virus-hits-every-member-of-population scenario indeed removes the burden of a single new gene in one organism having to takeover the population by reproduction and selection (thus bypassing Haldane-ReMine limits and random effects)…

    Thanks Atom.

    I guess I should be more specific too. DS bagan by talking apples. RV insertion in the oocyte:

    An objection was raised about how it was possible for a germ cell to become infected by an RV in the first place and secondly how could it survive the infection and go on to grow into a reproducing adult. … Egg cells however are a whole different story. In mammals a female is born with a lifetime supply of primary oocytes (immature egg cells) already created.

    Then when you raiseed your objection, which is still vaild, the switch to talking about oranges took place:

    … virus-hits-every-member-of-population scenario…

    IOW, he just relied on the same scenario, used it to answer an objection to his “RV in the EGG,” scnario, that his “RV in the EGG” scenario was supposed to resolve!

    Don’t let him get away with it. You were on the right track.

  34. 34
    scordova says:

    Mike 1962:

    Just curious, but why do you reject common ancestry if the arguments for it are formidable?

    I think the arguments against it are equally formidable. I see something of a stalemate.

    In contrast, this is not the case, for example, with OOL where the balance is pretty lopsided in favor of ID. There is no formidable argument for mindless OOL.

    The ID/OOL debate is lopsided, but the common design vs. common descent is not lopsided. I think creationist Todd Wood gave the most balanced viewpoint.

    Furthermore, it would be appropriate for me to confess something of a personal religious bias. Over the years, as skeptical as I’ve been of a literal interpretation of the Genesis account, I’m thinking it has a better and better chance of being correct each day.

    Plus, I think in time we may have emprical data which will help us decide one way or another. Solexa technolgy may hold the key.

    I will keep hoping the facts will fall in favor of special creation. I am willing to change my mind, but I certainly have my personal hopes and biases….

    Unlike some of my brethren, I would prefer to resolve the issue of common ancestry theoretically and empricially rather than theologically.

    So even if I have my religious beliefs today, one will hopefully never see me suggests my personal beliefs are equal to scientific arguments.

    As of today, I agree with creationist Todd Wood, in that from a scientic standpoint, the creationists certainly don’t have a slam dunk case over their front-loaded-common-descent counterparts in ID’s big tent.

    And personally, I’m at this time content to let us all be one big happy family under the big tent.

    Salvador

  35. 35
    Jehu says:

    In contrast, this is not the case, for example, with OOL where the balance is pretty lopsided in favor of ID. There is no formidable argument for mindless OOL.

    OOL is only one of the “four big bangs”.

    1’) the Cosmological (the universe “just popped” into existence out of nothingness).

    2’) the Biological (life “just popped” into existence out of a dead thing).

    3’) the Psychological (mind “just popped” into existence out of a brain).

    4’) and the Moral (morality “just popped” into existence out of amorality).

    Each of these “big bangs” tells us there is a God. And so the proverbial divine foot is in the door. Once the divine door is open all the implications of divinty are on the table and theological considerations become rational. Considerations about the meaning of life and why we are here are just as important, if not more so, than speculations abourt ERV’s.

  36. 36
    bFast says:

    Jehu, I wholely agree with you and the majority of the scientific community that cosmology is a big bang event. Life seems to clearly be a big bang event. OOL is currently a very strong supporter of ID whether the OOL scientists acknowledge it or not. One can surely argue that multi-cellular life was a big bang event.

    However, I think that anthropocentrism is the cause of the belief that psychology and morality are big bang events. Animals unquestionably have psychology — ask any dog trainer. Fish have much less of a psychology, but they still have a psychology — ask any fly fisherman. Morality is a bit harder to discern, it is even harder to define, yet I bet I could make a good case that animals have a moral sense and moral code. The morality of animals is certainly limited compared to our own, yet it is exactly the fact that theirs is lesser that proves that morality is likely not a big bang event.

  37. 37
    Jehu says:

    bfast,

    Animals do not have morals, they have instincts.

  38. 38
    idnet.com.au says:

    Did Dave Scot propose that a population gets infected by a retrovirus all at a similar time and thus the benefit endowed by the virus spreads widely.

    If this is tha case, then we should see many different insertion points in members of the same species, and this would negate RVs present at the same locus being evidence of common descent.

    I personally favor common descent, but I wonder if RVs are really viruses that have infected organisms or whether they are mostly signal sequences.

    The non protein coding DNA of marsupials shows a 20% difference when compared to placentals (cf 1% for protein coding sequences). This implies that the difference between placentals and marsupials is in the junk, and that it is therefore not likely that junk really is junk.

  39. 39
    Mung says:

    Atom,

    [An unnamed individual] presented as a response to [an unidentified criticism] of a prior scenario, which I shall term scenario A, a new scenario, which I shall term scenario B. When presented with an objection to scenario B, [unnamed individual] presented as a counter-argument scenario A.

    Am I the only one who noticed?

  40. 40
    Mung says:

    This implies that the difference between placentals and marsupials is in the junk, and that it is therefore not likely that junk really is junk.

    It implies no such thing. Why accept without criticism the premiss that the differences are to be found within DNA?

  41. 41
    gpuccio says:

    DaveScot:

    I have said many times that I have no problem with common descent, but still I keep an open mind about it, and I would like to really understand how much evidence really supports it.
    You very correctly point to ERV as the best evidence for common descent. I agree with you. But still, I would like to sum up some of the big problems which seem to arise when we consider ERVs as evidence of common descent. They have already been clearly elucidated in the previous posts of this thread, so I am only trying to gather them, and I would really be interested to know your opinion:

    1) How can we explain the fixation of a specific RV insertion in the genome? Atom has very well raised this problem. You answered that RVs, differently from genes, can invade genomes horizontally. That’s true, but others, like pk4_paul and idnet.com.au, have observed that, in that case, we would not observe the same insertions. It seems to me that any argument in favour of fixation is at the same time an argument against the value of RVs as evidence of common descent. In other words, we have one of two scenarios:
    a) RV insertions are truly random: then, if the RVs expand horizontally, they should be found at different loci in the same species, and obviously also in different species. But in that case how can we explain the fixation of a single insertion, so much so as to be transmitted from the common ancestor to the descendants?
    b) RV insertions are not random, and they happen at specific loci. So, the expansion in a species is horizontal, but it happens in the same locus. But in that case, the occurrence of the RV in different species at the same locus is no more valid evidence of common descent, because it could be explained, similarly, as an effect of non random insertion.

    So, I see a true difficulty here.

    2) By the way, it seems that there are many evidences in the literature that RV insertions are not random. Is not this fact detrimental to considering them as evidence of common descent?

    3) Moreover, if we admit that RVs, and also retrotransposons, could not be random parasytes, but rather instruments of DNA plasticity (there is some evidence of that too, in the literature), more or less utilized by intelligent information and/or intelligent designer(s), wouldn’t that be another strong argument against their mechanical interpretation as passive “markers” of a random process of information alteration?

    That said, I am really interested in this discussion. I don’t think that religious convictions should have any influence on our appraisal of the evidence. But we must never accept “easy” interpretations of the existing evidence, without considering the problems which may arise from them.

  42. 42
    gpuccio says:

    Mung:

    “It implies no such thing. Why accept without criticism the premiss that the differences are to be found within DNA?”

    I can well agree with you that the differences are not necessarily only in the DNA. I am personally convinced that the most important differences are probably elsewhere, although at present it would be very difficult to concieve what this “elsewhere” may be.
    But stil, some differences are certainly in the DNA. And, of those differences, most are certainly in the non coding DNA. The importance of non coding DNA in the regulation of life processes cannot be overemphasized. Not only it is supported by a lot of evidence, at many levels, but it is really almost a logical necessity. How can anybody with a minimum os sense believe that human DNA is formed for only 1,5% by information bearing code, and for 98,5% by junk? Such an idea is simply ridiculous.

  43. 43
    jerry says:

    Darrel Falk has a lengthy chapter in his book that discusses the evidence for common descent. Besides retro viruses, he discusses what are called pseudogenes and gives examples of deletion pseudogenes that are identical from species to species such as goats and cows and another deletion that exists in great apes but not in monkeys. Deletions are rare and a powerful evidence of common descent since identical deletions across species would indeed be a low probability event.

    Falk mentions what is called SINE’s or simple interspersed nucleotide elements that are common between various animals and one links whales with the hippopotamus. Just google “sine evolution” and there is a long article about the evolution of whales based on this concept.

    I haven’t been able to find much on SINE’s but maybe someone else here may have some insight to the importance of these DNA sequences and whether they are functional or not. Falk seemed to think they are not functional and thus just mistakes passed along because they are stuck in the middle of introns.

  44. 44
    DaveScot says:

    pk4_paul

    If this were the case one would not expect to see insertion points at identical locci if this were truly a random process. But I am aware that there is excellent evidence for preferential insertion points. The significance of this lies in the use of ERVs by Darwinists to argue for common descent. If insertion points occur at preferred locations and a retroviral outbreak occurs, one would expect to see the evidence for this not only in the same genomic locations within a species, but also perhaps for different species, as would be the case for primates who have very similar genomes. Identical preferred insertion points would explain the presence of ERVs at the same locations in two species having very similar genomes. This still would not explain why genomic junk would be preserved over geologic time periods and indicates a natural selection anomaly.

    Good points. RVs don’t often cross the species barrier for both biological (incompatibility) and proximal (little direct contact to spread the infection) reasons. Not airtight of course but enough to cast doubt on same virus inserting at same preferred point in two different species. Granted the same insertion point in individuals of the same species should be unlikely (preferred insertion points aside) but I think that might be made up for by a great many individuals being infected. Also a new species that splits off is ostensisbly going to subtend from a small number of reproductively isolated individuals in the parent population.

    This is fascinating to contemplate. However retroviruses leave a genomic signature behind by which they are identifed. In addition for an ERV to become a functional part of a eukaryotic genome we would expect to find promotor regions, an initiation site and required transcription factors enabling gene expression.

    Of course. Proviruses do include promotor and initiation sites. They couldn’t get the cell to express their genes otherwise.

    I’m not a believer in accidental causality and before one invokes selection to explain how an accident becomes deterministic I’d like a clearer indication that selection is not an ad hoc concept, that can explain both the retention of junk over geologic time, as well as slightly beneficial theoretical changes.

    Keep in mind this is just one bit of corroborating evidence. I mostly base a belief in common ancestry on a common genetic code, the law of biogenesis, and nested hierarchy. Another explanation for all these things is of course possible but anything I’ve seen appears contrived in order to accomodate young earth creation.

    A related interesting question lies in accounting for the origin of viruses themselves. From a Darwinian perspective they are problematic being host dependent.

    They seems to be a deep mechanistic relation between retroviruses and retrotransposons. The only thing substantially different is the former exits the cell to insert itself into other cells where the latter confines itself to a single cell.

  45. 45
    DaveScot says:

    You very correctly point to ERV as the best evidence for common descent.

    You misunderstood what I wrote. ERVs were just the final straw that broke the camel’s back, so to speak. What the Darwinian explanation can’t accomodate is saltation beginning with the mysterious and sudden appearance of the first replicating cells very early in the earth’s history and continuing all through the fossil record. It’s simply inconceivable that any chance & necessity mechanism can bridge the stark discontinuities. The dogged refusal of the fossil record to show a continuum of small changes leading to novel cell types, tissue types, organs, and body plans falsifies the chance & necessity hypothesis. Moreover the central dogma has completely crumbled at the microorganism level through the discovery of horizontal gene transfer, mobile elements, and epigenetics. All these mechanisms are now suspected of playing a role in the evolution of multicellular life as well. Some explanation other than chance & necessity is called for. C&N might account for more trivial adaptations that don’t involve novel cell types, tissue types, organs, and body plans. Either intelligent design (front loaded at the beginning or injected at intervals over the course of time) is one of those explanations and it appears to fit all the evidence very well. Process structuralism is another mechanism but it is lacking in support as it supposes that there are hidden laws of nature. Intelligent design doesn’t presuppose anything that doesn’t already exist – intelligent agency that can modify organisms at the genetic level is already proven to exist in the universe in one instance. That agency is us of course. To suppose there’s just one of anything is in opposition to the Copernican Principle so in following that principle I must presuppose there are other intelligent agencies in the universe with the same or greater capabilities than our own. Nothing supernatural is required to explain a design scenario. No laws of physics need to be circumscribed or unknown laws postulated. Another intelligence with biochemistry expertise predating humanity in the sphere of the causally connected universe is all that’s required. Of course it could be much more than that – the matter and energy we know about in the universe and can describe with our current understanding of physics appears to comprise only about 5% of what’s actually there. 95% of the stuff that makes up the universe, known only by its gravitational interaction with normal matter, remains uncharacterized. Who knows what lurks there.

  46. 46
    jerry says:

    Here is the comment I made last week about the possibilities of the origins of common descent. From the evidence I have seen it is fairly well established but we can disagree.

    I know of at least four categories of mechanisms for the cause of common descent and others may have additional thoughts.

    1. front loaded evolutionary information put into one or more genomes at some deep distant time and over the course of time the information in these genomes were triggered and produced the various species. I am certainly not very knowledgeable on this so others may have better insight.

    2. sudden large changes in the genome cause by natural means. In the last year there have been discussion about various authors who have pronounced neo-Darwinism dead and that changes happened this way. Some specific mechanisms for these sudden and rather large changes to the genome are proposed but essentially they are only hypothesized to exist. Others may have better insight on this.

    3. gradual changes over time which is the standard fare taught in all the textbooks and universities as neo-Darwinism. However, there is almost no evidence at all for this position. Darwin proposed it and nearly everybody has followed his lead and accepted it but with little proof and lots of contradictory information. It is an amazing intellectual position for so many to defend without any backup. By the way I just read Stanley Jaki’s pamphlet on Intelligent Design and Darwin and he makes the point of the lack of empirical evidence backing Darwin’s ideas and that exactly “zero” species have been documented to occur by the Darwin’s gradualistic approach. Jaki is very critical of ID but equally disparaging of Darwin. Though he says that Darwin’s ideas unified Biology and explains everything except for the problem of no empirical data which is crucial for science.

    4. agency interfered at various times to change the genome. This is again only inference from available information and the small probabilities of the changes that occurred could happen by natural means. The last is the ID position that this mechanism happened at least once in the past and probably more. This is anathema to science since it looks like the fairy god mother appearing every now and then to cause changes.

    Under each, common descent would be a reality but each provides very different implications and none has any empirical support.

    As I said there is no empirical evidence for any of them but in some instances, #4 looks very persuasive to myself. Just what these instances are, is open to debate but I will go with OOL as one definite one. But to biologists Darwin’s ideas are equally persuasive because they unify everything.

    In other areas some naturalistic mechanism looks persuasive such as what best explains the geo disparity of life.

    These are just my observations on this topic and also sometimes I think we operate with less than a half deck of cards when discussing these things. There seems to be a lot of relevant information out there that we are unaware of.

  47. 47
    Michaels7 says:

    If RV loci are “not random” could this be the result of passive defense mechanisms related to spatial sequencing of so-called “junkdna”?

    Decoy DNA?

  48. 48
    Michaels7 says:

    Dave,

    Thanks for simplification. I have questions if anyone wants to chime in.

    “Because the ERV serves no function it is not conserved by natural selection and is slowly mutilated by random mutations over millions of years until it is no longer recognizable as the strain of provirus it once was.”

    Is this not a conundrum later if “no longer recognizable.”

    “There may be preferred insertion points in the genome for the RV genes but if there are there are a great many potential insertion points.”

    This might be a passive defense?

    “The case for common ancestry is made by finding the same strain of ERV inserted at the same place (loci) in the genomes of closely related species such as different primate species.”

    Here is the conundrum mentioned earlier. If the provirus is “no longer recognizble” then how can they find the “same strain” across millions of years? This is conflicting observations of data.

    “The argument is that the RV infected a germ cell in a common ancestor and the ERV was then inherited by all the descendents. When the species splits or spawns a new species that is reproductively isolated each species has the ERV but, and here’s the key, random mutation changes each ERV differently. By comparing the differences in ERV sequences at the same loci in different species one can establish a rough date for the original infection in a common ancestor given a more or less average background rate of random mutation.”

    Again, how can they compare something that is supposed to be beyond recognition?

    I’m left thinking there are some broad assumptions being made again by the well utilized “time” component of Darwin.

  49. 49
    great_ape says:

    “I haven’t been able to find much on SINE’s but maybe someone else here may have some insight to the importance of these DNA sequences and whether they are functional or not.” –Jerry

    The verdict is still out on SINE function, IMO, even for the hard-core evolutionist. I sit the fence on this one and await further evidence. Others lean more one way or the other. It is clear that SINEs have, on occassion, been adopted for organismal functions. That is, particular SINE *instances* have been adopted for organismal function. That does not necessarily imply function to them in general, as a group. David Haussler’s group has perhaps shown this sort of instance exaptation most dramaticaly with the Coelacanth SINEs and their human remnants. However, it is just as clear to me that not *all* SINE insertions have a function. New insertions are happening all the time (1 in 50-100 human births) and the vast majority of these are lost by drift and never reach fixation. We know this. Many of the copies that are fixed have severely and systematically atrophied thru mutation, some almost beyond recognition. This strongly indicates a lack of organismal function for these many many SINE instances. The same applies to ERV instances, pseudogene instances, etc.

    The beauty of using ERVs, SINEs, pseudogenes, etc, as beautiful and effectively irrefutable evidence of common descent, however, is that as long as the insertion process is effectively random–and this can be empirically evaluated for the SINE in question–the logic of demonstrating common ancestry is virtually undeniable. It serves as my litmus test for who can and can not understand scientific evidence in this debate and/or can not evaluate it objectively. Outright denial of common descent once shown these data is tantamount to thumbing one’s nose to science as an approach to understanding nature.

    But in that case how can we explain the fixation of a single insertion, so much so as to be transmitted from the common ancestor to the descendants? –gpuccio

    gpuccio, the statistics roughly state that 1/2N such insertions (even if they are neutral), where N is the population size, will fix by chance alone. If a certain locus happens to receive an insertion, it has this small probability of fixation. With enough insertional hits, some insertions are bound to fix. Thus if species A is an ancestor to species B, B will share that same insertion at this locus.

    You raise a good question as to how a non-random insertion process might undermine the logic used above. It depends on in what respect it is non-random. There are many levels of this. Some retrotransposons, such as R2, home in on very specific sites in the genome that are limited in number. Thus they are very unreliable for phylogenetic purposes. Other ERVS/SINES/,etc, are nonrandom only in the sense that they prefer gene-rich regions or AT-rich regions, etc. In fact, the vast majority appear to be of this variety. This sort of non-randomness is very benign for the purpose of inferring common descent. So one must understand the properties of the SINE/ERV, etc, being used. Once done, however, I think that you will find that the reservations you have about using ERVs,etc as evidence for common ancestry hold no weight.

  50. 50
    bFast says:

    Michaels7:

    Here is the conundrum mentioned earlier. If the provirus is “no longer recognizble” then how can they find the “same strain” across millions of years? This is conflicting observations of data.

    It is my understanding that it takes about 100 million years for unimplemented DNA to become total mush. As the common ancestor between the chimp and human is presumed to be about 3-4 million years ago, an ERV marker that existed at the time of the split would be reasonably and detectably preserved over that period of time. BTW, we can ignore degradation in the marker prior to the split.

  51. 51
    DaveScot says:

    Micheals7

    Unrecognizability occurs gradually. Like randomly replacing letters in a paragraph. You can still recognize it as the same paragraph by a statistically unlikely set of matching letters. Eventually it becomes statistically unrecognizable. The degradation process takes place over millions of years such that you won’t find this except between species that have a common ancestor in the more recent past. It doesn’t provide any evidence of common ancestry between birds and mammals as that (supposed) split from a common reptilian ancestor was too long ago, but it should up between disparate species of birds and between disparate species of mammals. The more recent the reproductive split the better the match between the provirus remnants. Many other genetic elements follow this same course of increasing mismatches over time as do whole genomes but those don’t tend to rule out common design as their basis. ERVs do because they are external in origin – unique new genes that show up whole, functional, commonly, frequently, and without predecessors.

  52. 52
    DaveScot says:

    great_ape

    It serves as my litmus test for who can and can not understand scientific evidence in this debate and/or can not evaluate it objectively. Outright denial of common descent once shown these data is tantamount to thumbing one’s nose to science as an approach to understanding nature.

    Good test.

    I have a litmus test to determine scientific objectivity as well.

    The test is whether one first acknowledges that intelligent agency capable of manipulating genomic content for an express purpose is extant in the universe and second whether the Copernican Principle is applied to such intelligent agency to presume that such agency is not unique. Acknowledging the former but not the latter speaks to an unscientific agenda that is more religious in nature than scientific. The Copernican Principle is the central dogma behind The Enlightenment. Denying it in the case of intelligent agency but not elsewhere is ideological bias and one can’t reason with ideological bias. If these two items are acknowledged then at least the evidence can be objectively examined and reasonable inferences drawn from it.

    I consider myself a hardcore materialist. The only difference between me and design deniers is that I consider intelligent agency to be material in origin and thus something that must be considered as a possible explanation of phenomena in the material world.

  53. 53
    Patrick says:

    scordova

    I think the arguments against it are equally formidable. I see something of a stalemate.

    And what may those arguments be? If you’re busy links are fine.

  54. 54
    jerry says:

    great_ape,

    All the data serves to support common descent. With my consideraly more limited knowlede, I agree.

    However, none of it supports any mechanism for speciation. Would that be a proper non inference?

    Hence Jaki’s comment that Darwin’s ideas unify biology but there is zero empirical evidence for speciation by gradualism and in science normally zero empirical evidence is usually a killer.

  55. 55
    bFast says:

    Great Ape, DaveScot — good interchange. Great Ape, I totally agree with you that the evidence for ERVs provides a strong logical support for a common ancestry model. An inability to recognize that demonstrates an inability to understand the basics of logic.

    However, DaveScot presents every bit as valid of a point. Science’s determination to blindly reject the possibility that it can detect intelligent causation, and science’s determination to blindly declare, “we cannot detect intelligent causation without knowing the causal agent, therefore intelligent causation didn’t happen” is every bit as illogical as the issue you present. Let science rule out intelligent causation, and until science has ruled it out, let science openly acknowledge intelligent causation as a valid explanation.

    The best explanation we have for the big bang, by far, is intelligent causation. The best explanation we have for OOL, by far, is intelligent causation. There are numerous other evidenciary challenges that are most easily explained by intelligent causation — Haldane’s dilemma comes to mind.

    Great Ape, please use as high of standard when judging your own illogic that you use when judging others.

  56. 56
    gpuccio says:

    great_ape,

    thank you for youe clarifications, as usual very precise and useful. I am very interested to this subject, and I will try to improve my knowledge about it as soon as possible. I am extremely interested in everything about non-coding DNA, including retrotransposons, SINEs, pseudogenes, introns and so on. I am sure there are still many things to understand about that.
    For the moment, I am grateful of your input. I really can agree that much of the evidence you refer to is a very good indicator of common descent.
    I maintain, anyway, my opinion that the current criteria for function in non coding DNA are not appropriate, because I am convinced, although I cannot substantiate it at present, that the regulatory role of non coding DNA will be understood only in the light of completely new aproaches.

  57. 57
    Mung says:

    By the way I just read Stanley Jaki’s pamphlet on Intelligent Design and Darwin …

    Stanley L. Jaki is by far one of my favorite authors. His works are highly recommended to all. Where did you find this booklet? Is it available online?

  58. 58
    Mung says:

    I can be a bit thick at times, I’ll admit. But can someone explain how using the presence of some marker to argue for a recent common origin of two species, and then turning around and using a recent common origin of two species to explain the presence of that marker is not an exercise in circular reasoning?

    Just trying to grasp the logic of “common descent” reasoning. Carry on.

  59. 59
    jerry says:

    Mung,

    If you go to

    http://pirate.shu.edu/~jakistan/

    there will be link to a pdf file with Stanley Jaki’s books and pamphlets at the bottom.

    Then call 1-888-808-2882 which is the current telephone number for Real View Books. You can get a lot of his stuff there though some of his works are no longer in print. It took them a day to get back to me and about a 5 days to get the pamphlets and books.

  60. 60
    Michaels7 says:

    Dave, BFast,

    Thanks. I’m not fully understanding some issues. HIV is a recent virus to humans and chimps after the branching according to modern evolutionary thinking. How do comparative genomes stand up to scrutiny on this RV? Am I missing something? Why doesn’t HIV render moot such arguments that RVs are solid proof of common ancestory if HIV became present only in 1900s? Doesn’t it throw a wrench into the gears? That in fact RVs develop after branching and are shared?

    The nesting is in the virus and the variation depends upon species, but not sure how this can be counted up to common ancestory.

  61. 61
    PaV says:

    great_ape: “gpuccio, the statistics roughly state that 1/2N such insertions (even if they are neutral), where N is the population size, will fix by chance alone. If a certain locus happens to receive an insertion, it has this small probability of fixation. With enough insertional hits, some insertions are bound to fix. Thus if species A is an ancestor to species B, B will share that same insertion at this locus.”

    And the probability of extinction is 1-1/2N, which is quite high.

    Let’s look a little closer. You say that “If a certain locus happens to receive an insertion, it has this small probability of fixation. With enough insertional hits, some insertions are bound to fix.” Well, there would have to be 2N “hits” for fixation, rather than extinction, to take place. Now, there are about 3 x 10^9 loci, i.e., nucleotides, in the mammalian genome. For a population size of 100,000 (10^5), that means there needs to be 2 x 10^5 x 3 x 10^9 “hits” for ONE location to be “fixed” randomly. This number is 6 x 10^14, or almost 10^15 “hits”. That’s one million, billion “hits”—on the oocyte—for just ONE loci to become fixed. I’m not familiar with viruses, but this seems like an exceedingly large number of viruses—all of which have to find their way to an oocyte/germ line.

    Now, you say “hits”; but don’t you really mean “insertions”? (I can’t see how a potential insertion—if that’s what you mean by a “hit”—can substitute for an actual insertion when dealing with the probability of fixation of a particular insertion) And, if we’re talking about an oocyte, and talking about an exogenous retrovirus becoming “endogenous”, then doesn’t that have to happen all at once, i.e., in one generation? If that’s so, then that means if we have 2N “insertions” at one loci, then ONE of those “insertions” will stick (become fixed). Conservatively, a virus is 2,000 nucleotides long. Again, for a population of 100,000, 2N insertions represents 2 x 10^5 x 2 x 10^3 nucleotides all together, or, 4 x 10^8 nucleotides, which is 10% of the mammalian genome. So that means in one generation, the most ERV that could be “fixed” is likely no more than 5, representing 50% of the genome. So, if we’re talking about a “common ancestor”, how could there be more than 5 ERV’s in common between any two species?

    I think I’m being “objective” in all of this. I look forward to your response.

    And, finally, as was brought up in another post concerning ERV, if this insertion of, conservatively, 2,000 nucleotides occurs only in the oocyte, then how in the world does the DNA where this insertion occurs match up with the homologous DNA from the sperm DNA? If a one nucleotide difference can cause a frame-shift error, what will a 2,000 nucleotide shift cause? I don’t think anyone has given an answer to this yet. Maybe you would want to comment though.

  62. 62
    PaV says:

    As I’ve thought these numbers over, it seems we need to throw out population genetics here. “Fixation” means something entirely different here. Since the insertion takes place in the oocyte, and, if I’m not mistaken, the exogenous becomes endogenous immediately, then fixation is the same as insertion. IOW, the probability of fixation is one.

    There seems to be two options when it comes to these insertions: (1) the insertions happen at random locations within the genome, or (2) there are only specific sites within the genome where these insertions can take place. And there are three options when it comes to the frequency of insertions: (a) insertions can only take place slowly over time (many generations), or (b) many insertions can simultaneously take place within one generation, or, [c] insertions take place at all available sites all at once—in one generation.

    For the case, 1a, assuming that over time *different* viruses will attack the oocyte, we would end up with a variety of different viruses found in random locations. Starting with a common ancestor, no correlation would exist between separate lineages after a considerable amount of time has passed. For the case 1b, again assuming different viruses insert themselves over time, we would again find a variety of viruses (thought not as great) that are randomly located throughout the genome. However, starting with a common ancestor, even after a considerable lapse of time, some kind of correlation might be seen between the two divergent lineages. For the case 1c, using the same assumptions as before, even after considerable time, there would be a correlation between two divergent lineages, with the virus(es) being almost identical, and with the locations—though randomly dispersed throughout the genome—the same. The amount of “deterioration” of the virus (in the absence of conservative forces) would be larger the farther back the two lineages diverged, AND, the deterioration would be EQUAL for all homologous locations.

    For the case 2a, with the aforementioned assumptions, then for two divergent lineages we would see, first, in terms of the location of these viruses throughout the genomes of these separated lineages, we would see a pattern of the locations that would appear, when a small amount of time separates the lineages, to be somewhat at random as regards the two lineages, but which would appear to have a greater and greater locational similarity as the amount of lapse time increased since the common ancestor. So, after a fair amount of time, we would likely see locations that are similar between the two, but with viruses that are somewhat different, and which have different degrees of “deterioration”.

    For case 2b(same assumptions), after a very short period of time, virus locations would match up well between the two lineages, and the viruses and virus locations would match up well. The amount of divergence in terms of the types of viruses would be small. Over longer periods of time, these correlations would still hold up, but we would likely see a, more or less, uniform rate of “deterioration”.

    For case 2c (same assumptions), we would see the same as 2b, but with more uniformity in the types of viruses found at particular locations, and with more uniformity in the amount of “deterioration.”

    From what little I’ve read about ERV’s, which is mostly from the posts here, my hunch is that we’re dealing with case 2a, simply because it sounds like we’re dealing with locations that seem to match up, and even viruses that are the same and are also found at the same locations; and….the amount of deterioration is variable, almost highly variable.

    The implications of this being 2a is that we’re dealing with a genome that has “specified” locations within it—which begs the question “What is specifying the structure, and how?”—and, as to the question of common ancestry, that species which have diverged recently will show very little “deterioration” and considerable correlation of locations and types of viruses at those locations; while species that have diverged over a considerable amount of time would show variable amounts of deterioration (all the way from “lots” to “very little”), a greater amount of variation of the types of virus that make up the ERV’s, and a fair amount of variation in the locations of the viruses.

    My sense is that to nail down common ancestry between humans and chimps we would have to see a small amount of deterioration of the viruses, and a high correlation of both the types and locations of the viruses (based on there being little time lapsed between the common ancestor of both lineages). [Also, if “different” types of viruses, for whatever reasons, are limited in their ability to become incorporated in the oocytes, then the correlation between the “types” of viruses should be quite high.] I’m curious as to how that stands up to what is known of chimp/human ERV correlations.

  63. 63
    Bob O'H says:

    Well, there would have to be 2N “hits” for fixation, rather than extinction, to take place.

    No, you have forgotten that living organisms reproduce.

    Suppose there is a new mutation/insertion of ERV, and that this creates a new allele which is neutral. Then there is one copy. The individual carrying the copy will (try to) reproduce, so in the next generation there will be some copies. It may be that there are none, or one, or two, etc. The main point is that the number will be random, and not related to presence of the new allele (because it is neutral).

    If there are no copies, then the allele goes extinct. If there are more than one, then the frequency has increased. If there is only one, then the frequency remains the same. In the next generation, the same process occurs, with every individual trying to reproduce, and passing on their alleles. Hence, there is a chance that the frequency will increase again. This process will repeat, and so there is a chance that the allele will eventually increase to a frequency of 1 (i.e. becomes fixed). Note that no mutation is needed for fixation, after the first mutation event: fixation occurs simply by random changes in the allele frequency.

    That the probability of fixation is 1/2N is simply because there are 2N individuals, and the allele is neutral. For me the most elegant proof of this is to notice that neutrality means that the expected frequency in the next generation is equal to the present frequency (if you like, if you could repeat the process a lot of times, then the average over the replicates would equal the current frequency). This expected frequency carries forward, so the expected frequency 10, 20, 3000 generations hence is equal to the current frequency. Now, we know that fixation is inevitable in a finite population (ignoring recurrent mutations: we’re just dealing with drift here), so at fixation the expected frequency must still be the current frequency. This can only happen if the probability of a frequency of 1 is the current frequency, and the probability of a frequency of 0 is one minus the current frequency.

    So, when a mutation event occurs, the current frequency of the allele is 1/2N (where N is the number of individuals, and the assumption is that they are diploid). Hence this must be the probability of fixation.

    The short, technical, form of this argument is “it’s a Martingale with absorbing boundaries”.

    Bob

  64. 64
    PaV says:

    Bob O’H: “Suppose there is a new mutation/insertion of ERV, and that this creates a new allele which is neutral. Then there is one copy. The individual carrying the copy will (try to) reproduce, so in the next generation there will be some copies. It may be that there are none, or one, or two, etc. The main point is that the number will be random, and not related to presence of the new allele (because it is neutral).”

    Doesn’t the Hardy-Weinberg Law say that in an interbreeding population the total number of alleles stays the same from one generation to another? So how does the frequency of the EVR increase from generation to generation unless the EVR itself reproduces and reinserts itself, or if another exogenouse retrovirus infects an oocyte of another member of the interbreeding population?

  65. 65
    Bob O'H says:

    Doesn’t the Hardy-Weinberg Law say that in an interbreeding population the total number of alleles stays the same from one generation to another?

    No, it assumes it (by assuming no mutation).

    It also assumes an infinite population size, so that 1/2N=0.

    Bob

  66. 66
    PaV says:

    Bob: “No, it assumes it (by assuming no mutation).”

    But we don’t need “mutations” here. The ERV is already in place. Since we’re dealing with a virus that has reverse transcriptase, thus directly inserting itself into the genome, and since viruses can replicate and so can be present in substantial numbers in a particular oocyte, I just don’t see how population genetics applies here. I think my analysis in #62 is more applicable here. Frankly, it’s very hard to visualize what’s actually happening here.

  67. 67
    Bob O'H says:

    PaV – I agree that we don’t need new mutations. We can just assume that, once the ERV has inserted, it just sits there in the genome. Then, to ask whether it fixes, we have to ask how its frequency will change. This is precisely the sort of question population genetics asks.

    The reason we need population genetics for this is because it gives us the framework for thinking about the problem. I would honestly have to suggest that you learn some (John Maynard Smith’s textbook “Evolutionary Genetics” is a good start). Even if you’re going to disagree with the some of the conclusions, it helps all round if you know and understand the basics of the subject.

    Bob

  68. 68
    PaV says:

    Bob, I’m already fairly familiar with population genetics. What you’re arguing here is that this ERV (“allele”) will become fixed simply through neutral drift. But if the probability of becoming extinct is .99999, and its probability of becoming fixed is 0.00001, and if single mutational events only produce a deterioration of the allele—IOW, simple mutational events can’t “produce” the form of any ERV, only a corruption of it—then why would you expect fixation? Simple stochastic variations—which is the only thing we can presume since the ERV is at most selectively neutral—should bring about extinction, not fixation. How do you see a way around this?

  69. 69
    Bob O'H says:

    PaV – I would expect fixation because I know that 0.00001 is not the same as zero. So that, although most mutations do go extinct, a small proportion go to fixation. Indeed, the rate of substitution is independent of (effective) population size, because the rate of fixation is 1/2N, but the rate of mutation in a population is proportional to 2N (because the rate per individual is constant across individuals: actually, we only need a slightly weaker assumption).

    Therefore, we expect to see some neutrally fixed alleles in populations. It may take a long time, because the rates are low, but evolution has that time (well, unless you’re a YEC :-)).

    Bob

  70. 70
    MatthewTan says:

    DaveScot

    I just happened to read this:

    http://www.godandscience.org/evolution/junkdna.php

    “It was assumed that retroviral sequences in human DNA represented leftover genes from infection of retroviruses. However, a new study demonstrates that these sequences actually block the infection of human cells with certain retroviruses (70). So, now these sequences seem to posses a vital function.”

    70. Hatziioannou, T., D. Perez-Caballero, A. Yang, S. Cowan and P. D. Bieniasz. 2004. Retrovirus resistance factors Ref1 and Lv1 are species-specific variants of TRIM5. Proc. Natl. Acad. Sci. USA 101:10774-10779.

  71. 71
    jerry says:

    Bob, PaV,

    I have some questions because it seems like there is a lot of assumptions going on with ERVs and other DNA sequences that are supposedly non-functional and common across the species.

    I believe there is only one human genome, from a mixture of 5-6 people and only one chimp genome. So I assume that there are several hundred (maybe thousands?) of ERV sequences resting insides introns that are common between this one genome of each. And that is what the basis for all these discussions.

    I also assume there are thousands of other ERV’s that exist in each species and do not match up. Also since we have only one genome, it is hard to know if any of these ERV’s are consistent across all humans and chimps unless someone is doing research on particular parts of the genome of each species for this phenomena.

    It would seem a likely research effort would be to try to take certain parts of the genome that contain these ERV’s and see if they are present in people who have been isolated for several thousand years such as people from New Guinea or the Amazon rain forrest. Is anything like this being done?

    It seems like we may be discussing some small sample sizes and generalizing or then again maybe we are not.

    Also a related topic is how does an ERV make it into the genome. Is it through the female or the male or through both? Does the virus insert itself into the egg or sperm and then somehow get neutered by ending up in an intron. If so then this would have had to have happened a very large number of times for so many ERV’s to make it through the genetics filter into the entire population. If there is a thousand ERV’s common to the chimp and human then because of the large population sizes it would mean tens of millions/billions insertion events to get to a thousand making it into the entire genome.

    Is there any understandable discussion of all this?

    Thanks.

  72. 72
    DaveScot says:

    matthew

    I read the referenced paper and don’t see where it says the retrovirus restriction factors are generated from the expression of endogenous retrovirus genes.

    http://www.pnas.org/cgi/reprint/101/29/10774

  73. 73
    DaveScot says:

    I was looking for the basis of the same ERVs found at the same loci in different primates and found the following to be the basis for most of it:

    Differences in HERV-K LTR insertions in orthologous loci of humans and great apes.

    Unfortunately I don’t have access to the entire article but do have some questions. The common loci were established using primers that contained flanking sequences to ERV LTRs. First question: how was it determined that the flanking sequences weren’t part of that particular strain of provirus and second how was it determined that the flanking sequences weren’t preferred insertion sites that caused the same virus to infect both species at the same site instead of infecting a common ancestor? ERVs are known to cross the species barrier so the integrity of common loci inference is critical and can’t be due to preferred insertion sites.

    The answer might be in the body of the paper.

    I don’t have a problem with fixation of the provirus as I think natural selection is greatly overrated in its ability to reward the more fit allele over the neutral one – there’s more luck to what gets fixed than anything else. Natural selection is far better at killing individuals harboring harmful mutations than it is rewarding those with slightly beneficial mutations. What it does more than anything else is conserve the species within fixed bounds (largely cosmetic and scale changes) typical of the species’ range but not radically alter it outside those bounds. I’m still a saltationist and the modern synthesis just can’t plausibly explain saltation.

    Also, is there anything more recent establishing common loci for ERVs based upon actual whole genome sequence comparison of human and chimp (since both were completed after the publication date of this paper) rather than establishing it by primer sequences? It seems like the whole genome comparison would be superior as there should be a whole lot more correspondence in the region than just flanks of ERV LTRs.

  74. 74
    PaV says:

    jerry: “It seems like we may be discussing some small sample sizes and generalizing or then again maybe we are not.”

    I’m just stumbling through all of this as well. I have the very same question in my mind about how much is actually known species wide. That’s what’s so hard in trying to figure out the mechanism, since we really don’t know if it’s “fixed” throughout species or not. Is this spreading through “neutral drift”, as Bob is suggesting, or is the insertion mechanism effectively the same as “fixation.”

    DaveScot: “It seems like the whole genome comparison would be superior as there should be a whole lot more correspondence in the region than just flanks of ERV LTRs.”

    I agree with you. It feels like we’re flying blind without whole genome comparisons.

  75. 75
    Atom says:

    In light of the developing discussion on this page, I’ll repeat my advice from an earlier comment:

    …At the moment, I’d say it is better to be cautious when using ERVs as evidence [for] anything, since we are just beginning to understand their function and guess at their history.

  76. 76
    PaV says:

    I was looking around and found this from a 1999 paper. It is of interest based on the discussions we’ve been having:

    “RESULTS AND DISCUSSION
    Building Phylogenetic Trees from ERV LTR Sequences

    Endogenous retrovirus loci provide no less than three sources of phylogenetic signal, which can be used in complementary fashion to obtain much more information than simple distance estimates of homologous sequences. First, the distribution of provirus-containing loci among taxa dates the nsertion. Given the size of vertebrate genomes (.1 3 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14). Furthermore, integrated proviruses are extremely stable: there is no mechanism for removing proviruses precisely from the genome, without leaving behind a solo LTR or deleting chromosomal DNA. The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species, whereas younger proviruses are limited to more closely related species. In theory, the species distribution of a set of known integration sites can be used to construct phylogenetic trees in a manner similar to restriction fragment length polymorphism (RFLP)analysis.

    Second, as with other sequence-based phylogenetic analyses, mutations in a provirus that have accumulated since the divergence of the species provide an estimate of the genetic distance between the species. Because, for any given provirus, it is highly unlikely that there will be selection for or against any specific sequence, it is safe to assume that the rate of accumulation of mutations approximates the rate of their occurrence, with appropriate corrections for reversion. Analysis of closely related proviruses integrated at different sites should also reveal regional differences in mutation rates.

    Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A).Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication. Although it has been noted that the divergence between the two LTRs of an ERV can serve as a molecular clock (8, 15, 18, 25), there are no reported prior attempts to utilize the LTRs of individual ERV loci as a source of phylogenetic signal. Assuming that the LTRs of an ERV are evolving independently, at approximately the same rate, and in the absence of rearrangement events, a phylogenetic tree containing 5′ and 3′ LTRs derived from the same ERV locus is predicted to have a topology similar to that depicted in Fig. 1B. The most useful feature of the predicted tree is the separate clustering of the 5′ and the 3′ LTRs. The node joining the 5′ and 3′ LTR clusters must be the deepest within the ingroup, since it represents thetime of integration, when the two LTRs were identical. Furthermore, both clusters are predicted to have similar branching patterns as determined by the phylogenetic history of the host species, with similar branch lengths. Thus, each tree displays two estimates of host phylogeny, both of which are derived from the evolution of an initially identical sequence (compare the 5′ LTR and 3′ LTR clusters in Fig. 1B). As we shall see, deviation of actual trees from this prediction provides a powerful means of testing the assumptions and detecting events other than neutral accumulation of mutations in the evolutionary history of a species.”

    The paper’s address is : http://www.pnas.org/cgi/reprint/96/18/10254.pdf

  77. 77
    PaV says:

    Here’s another interesting abstract, which makes me think there’s nothing to really demonstrate here (read the last sentence):

    ABSTRACT
    HERV elements make up a significant fraction of the human genome and, as interspersed repetitiveelements, have the capacity to provide substrates for ectopic recombination and gene conversion events. To understand the extent to which these events occur and gain further insight into the complex evolutionary history of these elements in our genome, we undertook a phylogenetic study of the long terminal repeat sequences of 15 HERV-K(HML-2) elements in various primate species. This family of human endogenous retroviruses first entered the primate genome between 35 and 45 million years ago. Throughout primate evolution, these elements have undergone bursts of amplification. From this analysis, which is the largestscale study of HERV sequence dynamics during primate evolution to date, we were able to detect intraelement gene conversion and recombination at five HERV-K loci. We also found evidence for replacement of an ancient element by another HERV-K provirus, apparently reflecting an occurrence of retroviral integration by homologous recombination. The high frequency of these events casts doubt on the accuracy of integration time estimates based only on divergence between retroelement LTRs.

    The paper is : http://www.genetics.org/cgi/reprint/171/3/1183 (P.S., what’s the code for inserting html addresses?)

    < a href="url.com" > hotlink text < /a > remove spaces between <>

  78. 78
    pk4_paul says:

    An Ancient Retrovirus-like Element Contains Hot Spots for SINE Insertion might be worth a look.

    Vertebrate retrotransposons have been used extensively for phylogenetic analyses and studies of molecular evolution. Information can be obtained from specific inserts either by comparing sequence differences that have accumulated over time in orthologous copies of that insert or by determining the presence or absence of that specific element at a particular site. The presence of specific copies has been deemed to be an essentially homoplasy-free phylogenetic character because the probability of multiple independent insertions into any one site has been believed to be nil. Mys elements are a type of LTR-containing retrotransposon present in Sigmodontine rodents. In this study we have shown that one particular insert, mys-9, is an extremely old insert present in multiple species of the genus Peromyscus. We have found that different copies of this insert show a surprising range of sizes, due primarily to a continuing series of SINE (short interspersed element) insertions into this locus. We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.

  79. 79
    great_ape says:

    short on time, but a few points:

    The high frequency of these events casts doubt on the accuracy of integration time estimates based only on divergence between retroelement LTRs. –abstract cited by PaV

    LTR divergence (i.e. the amount of mutations accumulated in the regions that were identical upon insertion) serves only as one means to date the insert. The presence/absence of the virus across species is the most important bit of information in forming a phylogeny and inferring common ancestry. Dating the insert via LTR divergence is just added corroborating information. So undermining the reliability of dating via LTR divergence–not that I think this article does that totally–does not undermine the inference of phylogenies and common ancestry itself.

    Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.

    I remember when this paper initially came out. Its point was well-taken; there are some rare regions of mammalian genomes that appear particularly receptive to mobile element inserts. Subsequent work has shown that the level of homoplasy (i.e. non-ancestral identify) arising from these or other such processes is actually quite low. Otherwise phylogenies based on SINE inserts would be incongruous with those obtained by means of nucleotide divergence. This has not proven to be the case; they are quite consistent. See, for example, Alu elements and hominid phylogenetics Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12787-91

    Overall, there are some caveats in analyzing viral/SINE inserts that would make one refrain from being overly confident in an inference made from any single SINE/virus insert. But the point I think some of you are missing is these studies are generally done with several inserts. And common ancestry is the only (non-contorted/non-adhoc) way to make sense out of what the collective data are saying.

    I wish I had more time to clear up some of the confusion concerning population fixation, etc, regarding viral insertions. Don’t let the fact that it’s a virus (or LINE/SINE/etc) confuse you; it still boils down to basic population genetics. Just replace A/a alleles with INserted/uninserted alleles and you can largely treat them the same in how they respond to drift, selection, etc. Remember, though, that only viral insertions occurring in the germline are players in this process.

    Jerry, I’m not sure if males or female germ cells are more subject to viral inserts. Males are more prone to mutations in general, and there’s evidence from the LINE/SINE world that suggests more more insertion activity. Not sure about the ERVs and “wild viruses” though.

  80. 80
    PaV says:

    “Don’t let the fact that it’s a virus (or LINE/SINE/etc) confuse you; it still boils down to basic population genetics. Just replace A/a alleles with INserted/uninserted alleles and you can largely treat them the same in how they respond to drift, selection, etc.”

    The insertion of the ERV is non-random. Population genetics is based on random mutations. How can the same phenomena explain both situations? These viruses are considered selectively neutral, so how does selection have anything to do with it? And I don’t think what happens to an allele is the same as what happens to ERV’s since SNP’s, simple mutations, can be enough to turn a gene on or off, hence phylogenetic expression; whereas SNP’s only cause deterioration of the original sequences, which are themselves extrachromosomal and thus have no way to effect phylogenetic expression. These are separate worlds. Why treat them the same?

  81. 81
    pk4_paul says:

    Identification of insertion hot spots for non-LTR retrotransposons: computational and biochemical application to Entamoeba histolytica is another paper correlating DNA structure to insertion sites.

    Different parameters that probed structural, thermodynamic or nucleosome positioning features were employed in our computational analysis of target site sequences in order to detect unique features, which may be recognized by the invading retrotransposon (Table 2). This analysis showed that DNA structure is likely to be important for target site selection in many retrotransposons, although, of the features tested, none were common to insertion sites of elements in all genomes. The presence of unique DNA structure at insertion sites appears to hold both for site-specific and dispersed non-LTR elements. Similar observations with DNA transposons show that the requirement for specific DNA structure at the target site may be a common feature. The bacterial transposon Tn7 (35) and the D.melanogaster P element (25) are known to recognize optimal DNA structures, rather than specific sequences, for preferential insertion.

  82. 82
    great_ape says:

    Why treat them the same? –PaV

    Because the essential feature of the virus/SINE/LINE that is in question and relevant for inferring common ancestry and phylogeny is the presence/absence of the insertion. That is the allelic state. As I mentioned before, some of these elements indeed have a nonrandom insertion process, but the type of randomness involved is almost always benign for the purposes we’re discussing here (common ancestry, phylogenetics). It technical terms, homoplasy levels are minimal, and thus they make even better markers than nucleotide changes in many cases. The most frequent non-randomness associated with viruses/mobile DNA is the targeting a short stretch of DNA (e.g. TTAAA) or gc-richness or AT-richness, or the targeting of generally open/active chromatin states. Once it inserts, it becomes an allelic character, and whether neutral or deleterious, it behaves very much like a SNP, microdeletion, etc, in population genetics. There are some minor differences in their propensity for recombination with other such sequences, and for gene conversion, and they are more likely to be deleterious because they’re a bulky introduction to the local chromatin.

    In short, for all practical purposes, you can treat them the same in population genetics. The ways in which they are not the same do not undercut their utility. This is coming from someone whose used these as alleles in peer-reviewed population genetics papers.

  83. 83
    great_ape says:

    Population genetics is based on random mutations.–PaV

    Not so. Population genetics is based on the behavior of allele/character states in populations. These alleles can be neutral, nearly neutral, deleterious, or beneficial. These alleles can be introduced into the population by random mutation, migration, or even transgenics. Doesn’t matter.

  84. 84
    great_ape says:

    …is another paper correlating DNA structure to insertion sites –pk4paul

    What must be asked here is how common is that targeted DNA structure? If it is ubiquitous in the genome, as is often the case, then insertions are still “random” among those distributed locations. It’s just a matter of total target space available for insertion. If the target space is large enough, then the sort of nonrandomness you’re addressing is unimportant. It simply slightly raises the probability of homoplasy (i.e. sameness that is not due to ancestry)due to two insertions hitting the same spot, but the extent it does so can be empirically evaluated and is typically found to be minimal.

    In sum, several of you have discovered valid biological issues related to using ERVS/SINES/LINES as markers, but, when understood in their appropriate context, there is nothing here that even remotely detracts from the weight of the argument for common descent, as Davescot lays it out in the top post.

    If I find time, I will try to write up the best argument possible against the inference of common descent based on ERVs and the like. I’d draw upon all the nasty details and loose threads I’m privy to. I’ll invoke nonrandom insertions, etc. But–here’s the kicker–I’d be obliged to *also* have a coherent explanation of the existing data concerning insertion states and their distribution among related species. I predict that any such argument I could make, however sophisticated, would come across as patently absurd to anyone reasonably intelligent reader, given the number of awkward contortions that would have to be made to explain the data we have accumulated. Compared to the absurdities that would need be invoked to make a non-common descent scenario workable, the minor caveats discussed above about using ERVs as markers are utterly insignificant.

  85. 85
    jerry says:

    great_ape,

    Thank you for all the effort and I for one appreciate the effort to make this understandable for those us that are not knowledgeable in micro-biology.

    I agree that the data points very strongly to common descent. But does any of this data point to speciation by any particular mechanism? Does any of this for example, show how the chimp and the human lines could have formed or does it just show that they seemed to have a common ancestor at one point in time and how they diverged and formed different characteristics is still at best a guess.

  86. 86
    scordova says:

    I wrote:

    I think the arguments against it are equally formidable. I see something of a stalemate.

    Patrick asked:

    And what may those arguments be? If you’re busy links are fine.

    1. Common Descent is questioned for cellular evolution (See Woese: “The time has come for biology to go beyond the Doctrine of Common Descent.” Front loaded ID could explain some of this, but why would a designer be constrained to front load a single invention?

    How far then can we go up the tree of life and saw away at common descent if common descent is not true for cells? If common descent of cellular evolution is doubted by a Darwinist like Woese, what else may fall?

    Now it is possible, dare I say probable there is a lot of common descent. I believe there is. Even modern YECs believe there is. The question is a matter of degree, not whether there is some common descent. It may well be Darwin argued against a straw man when he argued against “fixity of species” since there seemed to be the notion of change amonst creationists in Darwin’s day……

    A link I think is a good starting point is:

    Should We Stop Criticizing the Doctrine of Universal Common Ancestry? by Jonathan Wells

    and

    Is Common Descent an Axiom of Biology? by Paul Nelson

    I thought creationist Todd Wood did a good job pointing out evidence in favor of common ancestry of humans and chimps. I respect his honesty and I think creationists will do well to acknowledge the issues Wood raises.

    I think it appropriate to give the scientific method a chance to resolve the issue eventually. I don’t think either side of the issue has a slam dunk case. I hope both sides will exercise mutual respect, especially under the big tent.

    And on another note, I’m skeptical of mainstream paleontology, cosmology, and paleo geology. These fields are infested with speculation and pseudoscience.

    The fields of science I have regard for are opreational scientific disciplines from which we have modern medicine and modern technologies. I consider these trustworthy scieces. After all, we have entrusted our lives to these sciences.

  87. 87
    great_ape says:

    But does any of this data point to speciation by any particular mechanism? –Jerry

    To my knowledge, none of this data speaks directly to mechanisms of speciation. And I certainly am not claiming that ERVs/SINEs provide a strong argument against ID itself–particularly since we still may have much to discover about their biological properties–I’m simply saying that they are a powerful argument for common descent and against YEC. A decisive argument in my opinion.

    …or does it just show that they seemed to have a common ancestor at one point in time and how they diverged and formed different characteristics is still at best a guess?

    I think that’s a fair assessment.

    To qualify, though, sometimes (we believe based on data) ERV/SINE insertions are commandeered and are a component of the divergence process.

  88. 88
    Mung says:

    The insertion of the ERV is non-random.

    Irrelevant.

    Population genetics is based on random mutations.

    False.

    Population genetics is based on initial frequency of the allele, the size of the population, and the “fitness” or “selective value” of the allele.

    How can the same phenomena explain both situations?

    What a confusing (confused?) question.

    From Wikipedia:

    By the explanandum, we understand the sentence describing the phenomenon to be explained (not that phenomenon itself); by the explanans, the class of those sentences which are adduced to account for the phenomenon (p.152).

    Population genetics is based on the behavior of allele/character states in populations. These alleles can be neutral, nearly neutral, deleterious, or beneficial. These alleles can be introduced into the population by random mutation, migration, or even transgenics. Doesn’t matter.

    That’s more like it.

  89. 89
    scordova says:

    Patrick,

    One of my comments to you just got released from the spam filter.

    Sal

  90. 90
    DaveScot says:

    great_ape

    I was hoping you could respond to my comment 72 asking for whole genome comparisons of othologous loci. The only thing I was able to find in how orthologous loci for the same ERV in different species are identified was DNA amplification using primers with viral LTRs and flanking sequences thought to not be part of the provirus. This was done before whole genome sequences were available. The same search for orthologous loci can now be done entirely with something like BLAST using whole genome databases and nothing more. Has this been done? It could reveal flaws in the assumptions underlying the inferences drawn from othologous loci or it could serve as even stronger evidence in support of them. It would certainly be superior to DNA amplification techniques.

  91. 91
    great_ape says:

    Davescot,

    Such studies have been conducted for SINEs/LINEs in apes…I think ERVs as well, but I need to rescan the literature to refresh my memory. I think Eichler’s group did an ERV study a few years back. I’ll double-check the literature and post back here. One reason such completely in-silico studies might be scarce is that it requires at least 3 species’ sequences from the same Order. We now have that with human-chimp-macaque, for instance, but that’s an unusual case. Two species don’t really allow you to infer much without consulting a third, and this until recently was done via PCR so the number of loci examined were modest.

  92. 92
    PaV says:

    great_ape: “Once it inserts, it becomes an allelic character, and whether neutral or deleterious, it behaves very much like a SNP, microdeletion, etc, in population genetics.”

    Well, one of the things that separates the insertion from a SNP is that the insertion can only take place at certain sites (apparently). SNP’s can occur anyplace. Leaving this distinction aside for the moment, for fixation of this insertion to take place, according to what you’re proposing, the ONE individual in this population of 100,000 that has a particular insertion at a particular locus on one of its two chromosome pairs is, randomly going to overtake the 99,999 individuals who, at this very same locus, have the very same nucleotide base. How is it all reasonable to assume that this ONE different component—and NEUTRAL at that—is going to overtake the other 99,999 homozygous nucleotide bases that exist at the same locus? If you start saying…..“Well, if this ONE has a lot more offspring than the others……” Well, isn’t it possible, and reasonable to assume, that there will be lots of the 99,999 individuals without the insertion that will have even more offspring (as paired mates) than this ONE? Really, it strikes me as preposterous to assume that ONE in 200,000 is going to swamp the other 199,999 rather than the 199,999 swamping the ONE. And bear in mind that one of the things that Fred Hoyle quickly points out is that populations have to be “normalized”. Another way of saying that is that in nature we see, more or less, stable populations. What that means is that over significant periods of time, on average, any two mating animals will give rise to two members of the population. Seen in this fashion—which corresponds to nature itself—on average, the ONE insetion will give rise to ONE insertion. But because of stochastics, it should quickly disappear. That’s why the probability of extinction is so high.

    The way population geneticists deal with the huge improbability of fixation is to say, “Well, if you have 2N insertion events, then one of them will become fixed. The problem with dealing with insertions, though, is that we don’t know really know what the mechanism is for these kinds of insertion. Yes, it is supposed to be through the maternal cell line, but we don’t have an insertion rate into the genome. This makes it almost impossible to assess the situation.

    So, let’s leave the insertion to the one side, and simply ask ourselves what the numbers look like for the fixation of a SNP at a particular locus in the genome since we have some idea what the mutation rate is for SNP’s. The mutation rate is roughly 1 x 10^-8. To calculate the rate of the same SNP occurring at the very same location in the genome (the condition for building up to the 2N needed mutation events) is: (1 locus/3 x 10^9 nucleotide bases) x (10^-8 mutations/base replication) x (3 x 10^9 nucleotide bases per replication=generation) x ¼ nucleotide base options= 2.5 x 10^-9 identical nucleotide base replacement at locus “x”/generation. For an entire population, there would be 2N such replacements taking place per generation, so that we have a rate of replacement, for the population, of 2N x 2.5 x 10^-9 replacements/generation, which, for N= 10^5 means 5 x 10^-4 replacements/population/generation.

    But we need 2N such replacements for fixation. So how many generations of this population are necessary for these 2N replacements to take place? Well, for a population of 10^5, that means 2 x 10^5 replacements x 1 generation/5.0 x 10^-4 replacements = 4 x 10^10 generations. Assuming, conservatively, a generation takes one year, then this represents 40 billion years. Thus, we conclude that if we treat this insertion as a SNP, then it is impossible for the insertion to become fixed. Isn’t this proof that insertions and SNP’s are entirely different?

  93. 93
    PaV says:

    Population genetics is based on random mutations.–PaV

    great_ape: “Not so. Population genetics is based on the behavior of allele/character states in populations.”

    I was contrasting the non-randomness of the insertions with the randomness of either recombination events or SNP’s, etc.

    I ask you, would Kimura have written his book on the Neutral Theory if random mutations didn’t exist?

    Here’s what Wikipedia says: “Population genetics is the study of the allele frequency distribution and change under the influence of the four evolutionary forces: natural selection, genetic drift, mutation, gene flow and selective mating.” Take away mutations and what have you left? So, I hope we can stop with the pedantry. (That includes you Mung)

  94. 94
    PaV says:

    Oops! I really should be more careful! The final number in #92 should be 0.4 x 10^9, or 400 million years. Again, an almost virtual impossibility for the fixation of an ERV insertion into a mammalian line, and a death knell, it seems to me, of the neutral theory.

  95. 95
    DaveScot says:

    PaV

    If not germline infection then how do you propose all those ERVs became fixed by the thousands in the genomes of each of many vertebrate genomes examined so far?

    I’ve yet to hear any other plausible explanation and absent that the germline infection hypothesis is the only game in town.

  96. 96
    Atom says:

    DS

    I’ve yet to hear any other plausible explanation and absent that the germline infection hypothesis is the only game in town.

    How about “we don’t know yet”?

    In the words of John Baez:

    But, the “only game in town” argument is still flawed.

    Once I drove through Las Vegas, where there really is just one game in town: gambling. I stopped and took a look. I saw the big fancy casinos. I saw the glazed-eyed grannies feeding quarters into slot machines, hoping to strike it rich someday. It was clear: the odds were stacked against me. But, I didn’t respond by saying “Oh well – it’s the only game in town” and starting to play.

    Instead, I left that town.

    It’s no good to work on string theory with a glum attitude like “it’s the only game in town.” There are lots of other wonderful things for theoretical physicists to do. Things where your work has a good chance of matching experiment… or things where you take a huge risk by going out on your own and trying something new.

  97. 97
    PaV says:

    “If not germline infection then how do you propose all those ERVs became fixed by the thousands in the genomes of each of many vertebrate genomes examined so far?” DaveScot

    I’ve been scratching my head a lot (and still continue to do so), and the only thing that makes sense to me—and I think it’s reasonable to think so—is that you have an infection that effects the majority of the population all at once. I’m thinking that if, e.g., 75% or more of the germ line was infected all at once, that from there, just due to randomness, it’s possible for an ERV, at a particular site, to become fixed, and thus serve as a ‘marker’. That’s the best I can think of. As I said, I continue to scratch my head. (It would make a big difference, of course, if we knew how the original, let us say, “infection” of the germ line occurred. I’m not aware that anyone knows that.)

  98. 98
    PaV says:

    A caveat to what I just posted is the fact that there appears to be numerous preferred (non-random) sites where ERV’s can happen. So even if there were a massive infection taking place in a population, in order to arrive at a fixed ERV at a fixed site, we would probably further have to add that the particular infection that invaded the germ line, also, in some way, had a preference for a particular site. While this is plausible, I wouldn’t want to say it’s probable. I have to run…..

  99. 99
    DaveScot says:

    atom

    How about “we don’t know yet”?

    I think I’ve been careful to call it a hypothesis rather than a theory. In the literature it’s often qualified as a presumption. Just because something isn’t proven doesn’t mean we can’t presume something is correct. Nobody actually saw South America and Africa connected together at one time. Nobody saw meteors making all the craters on the moon. Nobody has gotten a sample of the earth’s core to prove it’s molten iron, and so forth.

  100. 100
    Atom says:

    DS,

    True, but if there are problems with the “only game in town” presumed explanation (assuming that PaV’s assesment is correct), then I’d rather stick to the “I don’t know at this point” approach. Maybe that’s just me. (Like John Baez, I leave that town for the time being.)

  101. 101
    DaveScot says:

    Orthologous loci in different species might be explained by the same virus infecting different species at the same preferred insertion point but there doesn’t seem be much room for dispute in how ERVs find their way into heritable DNA – the same way they get into somatic DNA – by invading a cell and reverse transcription. It’s a classic smoking gun. Means, motive, opportunity, and weapon. An eyewitness is all that’s lacking. That’s still enough to get a conviction and a death sentence.

  102. 102
    PaV says:

    great_ape, is there anything wrong with the mathematics I used above? I’d be interested in where I might be wrong.

  103. 103
    jaredl says:

    I am ignorant, and ask for help.

    If two separate cells from the same individual were to become infected by the same type of ERV, how would the genetic material from the ERV become incorporated into the host DNA, and would the ERV infect the same loci in the host genome of both cells? What gets the ball rolling, precisely?

  104. 104
    great_ape says:

    hi all,
    tied up at work for the moment; will post reply to your questions later this evening.

  105. 105
    great_ape says:

    ERV phylogenies and some references:

    It occurred to me after my earlier post that, in addition to PCR-amplifying the same locus from different species to assess insertion status of ERVs,
    the PCR products are also sequenced in almost every such study. The sequence shows accumulated nucleotide differences
    that are themselves informative and can rule out contamination issues, etc, that might otherwise confound the results. So I think that,
    with the notable exception of the smaller sample size, these studies are just as good for proving the point. As we get a denser sampling of full genomes, the sort of in silico comparisons you’re looking for will be available (see macaque paper below), but below I list the closest thing so far that I’ve come across. I think there is more
    from the rice genomes comparisons as well.

    This one is a bit dated but freely available. It’s not a whole genome study, but it is a good example of what has been done:
    Constructing primate phylogenies from ancient retrovirus sequences
    Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10254-60.

    Here is a companion paper to the macaque genome that did a whole genome comparison of ERVs, SINEs, and LINEs Unfortunately it requires a Science subscription. Some Highlights, though:
    “Similar to the human genome, the rhesus macaque genome contains over half a million recognizable copies of endogenous retroviruses (ERVs) and their nonautonomous derivatives,
    with the great majority being present or fixed before the hominoid-OWM split”
    In other words, most of the ERV are shared at the same location in both
    humans and macaques. (The same goes for LINEs and SINEs.) For ERVs, both human and macaque show ~3500 new insertions that have fixed
    since the separation of the lineages. For any of these (500,000 – 7000) shared ERV insertions, the complete and unambiguous absence of the insert at the orthologous location in the chimpanzee genome would, in principle, be evidence against common descent. (There’s a YEC research program for you, by the way, any takers?) At the end of the day you’ll find 99.99% of inserts support common descent. Sometimes stubs are left behind where the LTRs are recombined out. Sometimes the entire locus may have been lost in one or more species making analysis impossible. You might find a few blips, but the overwhelming majority will be consistent with the hypothesis of common descent.
    Hard to ask for much more in the way of support.

    reference:
    Mobile DNA in Old World Monkeys: A Glimpse Through the Rhesus Macaque Genome
    Science Vol. 316. no. 5822, pp. 238 – 240

    Here is the the great ape phylogeny from the same group using SINE insertions:
    Alu elements and hominid phylogenetics.
    Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12787-91. Epub 2003 Oct 15

    Here is an old world monkey phylogeny based on SINE insertions. It is in agreement with the phylogeny based on nucleotide divergence. Common descent is the only plausible explanation for this.

    A mobile element based phylogeny of Old World monkeys.
    Mol Phylogenet Evol. 2005 Dec;37(3):872-80. Epub 2005 Jun 3.

    Perhaps there’s someone lurking, also, that knows of additional refs that would be useful outside the mammalian world.

  106. 106
    great_ape says:

    hmmm.. My latest post may have gotten hung up in the spam filter because of the refs included…

  107. 107
    great_ape says:

    Population genetics is the study of the allele frequency distribution and change under the influence of the four evolutionary forces: natural selection, genetic drift, mutation, gene flow and selective mating
    Take away mutations and what have you left? –Pav

    You do realize that we can still read the text that isn’t bolded, don’t you? I count 3 forces remaining when mutation is removed. And I don’t see any specification of “random” mutation as opposed to any other kind. That’s because the study of population genetics is about the polymorphic marker, not its origin per se. So, all pedantry aside, your original statement is still very much wrong regardless of which parts of the definition of population genetics that you bold for emphasis.

  108. 108
    great_ape says:

    according to what you’re proposing, the ONE individual in this population of 100,000 that has a particular insertion at a particular locus on one of its two chromosome pairs is, randomly going to overtake the 99,999 individuals who, at this very same locus, have the very same nucleotide base –Pav

    Pav,
    Going thru your math and reasoning is going to take a moment, but I’ll address where I believe you have gone astray later tonight. Hopefully my earlier post that’s stuck in the filter will get thru by then.

  109. 109
    great_ape says:

    Pav,
    Here’s my assessment of your analysis:
    #1 Well, one of the things that separates the insertion from a SNP is that the insertion can only take place at certain sites (apparently) –PaV

    Yes, but that’s still leaves a lot of possible sites for insertion by any given ERV sequence. It’s very rare for a virus to have a specific/unique target preference in the DNA. We can recover insertion loci from experimentally infected cells. That is, we can find out where they inserted. The integration process is still effectively random with respect to location. You needn’t take my word for it. Look up papers that have experimentally examined where retroviruses inserts. There can be hotspots, yes, but in general it’s pretty sporadic. You must be able to make the distinction between something not being random with respect to every factor, yet still being random with respect to the issue at hand. This is a common sticking point. I used to think people were conflating the different meanings of random for rhetorical purposes–and I’m sure some folks do–but I now think that many people are just confused.

    #2 …according to what you’re proposing, the ONE individual in this population of 100,000 that has a particular insertion at a particular locus on one of its two chromosome pairs is, randomly going to overtake the 99,999 individuals who, at this very same locus, have the very same nucleotide base

    a) Not exactly. That one inserted allele of that particular genomic locus is going to overtake all the other non-inserted locus. Because of recombination, we’re not dealing with individuals in population genetics. b) the effective breeding population size of humans is estimated to have been around 10,000 longterm in the relevant time period. c) you don’t have to believe me; it can be demonstrated mathematically (P=(1-e^(-4Nsq))/(1-e^(-4Ns)) (shown by Kimura; where q is the initial frequency of the allele, N is effective population size, and s is the selection coefficient (for our purposes it’s zero)). and by simulation that the probability of any one such allele beating out all other such alleles is 1/2N (in other words, its initial frequency). So, for every 20,000 germline insertions of ERVs (that go on to form a zygote), roughly one would fix simply by neutral drift in ancestral humans.

    (continued)

  110. 110
    great_ape says:

    (continued from above)

    #3. Another way of saying that is
    that in nature we see, more or less, stable populations. What that means is that over significant periods of time, on average, any two mating animals will give rise to two members of the population. –Pav

    a) This isn’t true of animal populations today nor is there any reason to believe it has been true in the past. Hence extinction. b) Even if it were true, it would be largely irrelevant for the purposes of our discussion. Gametes are sampled each generation by and can produce drift even under stable population sizes.

    #4. “…Well, if you have 2N insertion events, then one of them will become fixed. The problem with dealing with insertions, though, is that we don’t know really know what the mechanism is for these kinds of insertion.

    We know a fair amount about how viruses insert. Certainly there are some details left to work out, but arguing that this rules out the 2N insertions yields one fixed events is an extreme example of retreating into a gap in knowledge to prevent yourself from accepting the inevitable conclusion. There are studies examining patterns of viral integration, both in the wild and in cell culture.

    #5 [assundry calculations] Isn’t this proof that insertions and SNP’s are entirely different?

    The short answer is no, but I’ll elaborate a bit. When your math involves one generation a year and still demonstrates a SNP would take 40 billion years to fix in a population size of 10k, it’s safe to assume a wrong turn was taken somewhere along the way. There are a number of ways to approach this issue, some more complex than others, I give the crude abridged version below.

    To calculate the rate of the same SNP occurring at the very same location in the genome…
    Why exactly would you want to calculate it for the same location in the genome? Where the SNP or ERV insertion occurs is irrelevant. This is the first indication that something has gone wrong.

    Let’s use the human per site mutation rate from Nachman and Crowell (2000) of 2.5 x 10-8 mutations per nucleotide site. (175 novel mutations per diploid genome per generation).

    The number of base replications is already taken into account in the mutation rate so your second 3 billion term is redundant.
    The probability of mutating to the same base is taken into account already in the way observed mutation rate is calculated, so that term is also redundant also. (The math for nucleotide transition models that calculate probability of identity and nonidentity at a locus as a function of time is more complex; see a good popgen or molecular evolution text for details on transition models if you’re interested).

    If you calculate that out, you get roughly 175 novel nucleotide (SNP) mutations in each newborn individual. Crudely, that’s about 1,750,000 novel nucleotide mutations in a given generation in a population of 10k breeding individuals. So clearly that’s enough such that we’d expect at least a number of those new mutations (assuming its neutral) to ultimately fix in the population/species. (1.75 million / 20,000 yields 87.5 lucky nucleotide variants that will reach fixation) Now, of course, there are many such generations and not every change will be neutral.

    Now what’s the situation for ERVs/SINEs/LINEs. Mutation rates are less well defined and certainly much more variable than the biochemical processes underlying nucleotide mutation. Current estimates for LINE/SINE insertions are on the order of 1 insertion per 50 to 100 births. These estimates are made, in part, by observations of the number of de novo insertions disrupting genes and causing disease, but other methods are used as well. The number of fixations when looking at chimp/macaque, etc. are concordant with that figure.

    ERV data is less clear. There are about 3500 ERVs that fixed in humans since the human lineage diverged from macaque. I’m guessing less than 1000 since chimp, but I’m not certain. Let’s use 750 as our number of fixed ERV insertions since the . What would the ERV germline insertion rate have to be to come up with this figure since, say, human and chimpanzee diverged? Roughly 750 * 20k = 15 million insertions. Sounds daunting. But let’s run the numbers. How many folks do we have to work with? That’s 240,000 twenty-five year generations over roughly 6 million years or 10k humanish things per generation crudely yields 2400000000 births. So that roughly 1 ERV insertion in every 160 births (or, rather in the germ cells that yield the birth) to support current genomic observations. Not crazy, particularly given that viral outbreaks could have caused the germline insertion rate to shoot up wildly during some parts of history. I ran through this quickly, so I may have screwed up something, but the take home message is that you don’t need astronomical numbers/time to get the kind of fixation rates we’re talking about.

  111. 111
    PaV says:

    Looks like a post is in the spam filter. Before addressing your response, there is a clarification or two that is needed.

    The language that has been used concerning the ERV’s has suggested a.) that we’re dealing with fixation, and b.) that we’re dealing with fixation at a *particular* “hot spot”.

    As to a.), I’ve read a paper that is basically using information that comes from the human genome project, and other sequencing work. But how representative is that data for entire species, whether human, baboon, orangutan, or chimp? If we’re dealing with limited genomic sequencing—which I suspect to be the case—then in what way can we say that “fixation” has taken place? It seems to me that the most one can say is that the *allelic* frequency is at least such and such—and no more.

    As to b.) it would appear that certain ERV’s just happen to appear in certain chromosomal locations, and, based on a specific sequence, and a BLAST survey, these locations are identified. This suggests to me that there is no *particular* location where the SAME ERV is located itself. If so, this completely changes the kind of thinking that’s needed.

    I would appreciate your take on these two points before we proceed any further.

  112. 112
    great_ape says:

    The language that has been used concerning the ERV’s has suggested a.) that we’re dealing with fixation –PaV

    Agreed.
    b.) and..that we’re dealing with fixation at a *particular* “hot spot”.

    Not really. We can talk abstractly about a single spot, but the data concerns lots of ERVs having fixed in lots of spots. And the experimental (cell culture) data concerns lots of viruses inserting in lots of different spots. So focusing on a single “hot spot” is not very helpful IMO given that we are dealing with how ERVs generally behave in genomes and populations.

    If we’re dealing with limited genomic sequencing—which I suspect to be the case—then in what way can we say that “fixation” has taken place?

    Sampling size can be an issue for some purposes, but for the most part does not affect the inferences we’re making here. The genome sequence is a single or at most an amalgam of a few individuals. So it is indeed a small sample. Yet fixation is determined or inferred by a number of means. In some cases a large sample of the population is tested for the locus. If all of 100 geographically diverse people have the insert, its very likely that its fixed. Not 100% certain, but pretty likely. In other cases, if two distant species share the same insert, and the (presumed) time since speciation is very long, then fixation is inferred because (barring very rare circumstances) an allele can (statistically speaking) only remain polymorphic for a limited period of time before it is either lost in one population or fixed. So if a long time has elapsed and the species share an insertion, fixation is inferred. In addition to the speciation time, a long interval of time can also be inferred by the accumulated mutations in the ERVs themselves. (In humans the average coalescence time at a given locus (i.e. how long before its completely replaced by some individual allele) is around a million years if I’m not mistaken. This is a function of population size. So ERVs that are present in both macaque and humans at the same spot will be extremely likely to be fixed in both species)

    This suggests to me that there is no *particular* location where the SAME ERV is located itself. –PaV

    I don’t understand this last point, perhaps you could try restating it some other way.

  113. 113
    PaV says:

    This suggests to me that there is no *particular* location where the SAME ERV is located itself. –PaV

    You’ve basically answered my question when you said earlier that “we can talk abstractly about a single spot, but the data concerns lots of ERVs having fixed in lots of spots.”

    As far as fixation, I appreciate the explanation and the statistical means used. You then say:
    “So ERVs that are present in both macaque and humans at the same spot will be extremely likely to be fixed in both species)”

    In the paper I read, which used the LTR’s in assessing integration times, etc, it didn’t seem to me like they were comparing ERV’s that are present at the same spot in both humans and macaques. There’e no explicit indication of that. Is that simply to be implied? In the paper they compare the 5′ and the 3′ LTR’s. It seems that the 5′ LTR is from the “host” and the 3′ LTR is inserted with the ERV. Is that a correct inference?

  114. 114
    corrado says:

    Dave,
    your article of May 10 only recently came to my attention.
    I disagree with your statement that “As it turns out it probably isn’t very likely at all for sperm cells to be either infected with a provirus or survive the infection. ……. They are also very active cells and even if infected would likely be hobbled enough to not be successful at fertilizing an egg.”

    Sperm cells of virtually all animal species are axtremely permeable to foreign DNA or RNA sequences that can be taken up after ejaculation when spermatozoa are exposed to the environment and delivered to oocytes at fertilization. Exploiting this spontaneous feature, spermatozoa have been used as vectors to introduce new genetic traits in various animal species. In addition, spermatozoa are endowed with an endogenous reverse transcriptase activity that allows to reverse transcribe in cDNA copies exogenous RNA molecules that are taken up.
    If these events can take place occasionally in nature they can be regarded as a potential source of mutation in the host genome with some relevance for the evolutionary processes.
    You may have a look at the following review articles:
    1. C. Spadafora Sperm cells and foreign DNA: a controversial relation. (1998) BioEssays 20, 955-964
    2. K. Smith and C. Spadafora Sperm-mediated gene transfer: applications and implications (2005) BioEssays 27, 551-562

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    Medicodon says:

    I am looking for documentation in the scientific literature of a particular ERV integrating at EXACTLY THE SAME LOCUS IN EXACTLY THE SAME POSITION in two different species. Could you (or anyone else) direct me to an article or study that shows this?

    Best regards,

    MD (board certified radiologist)

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