Endogenous retroviruses

[Loudmouth]

The focus is on the LTRs because that is about all that is left.

And these LTR's are viral in origin and are heritable, which makes them a viable candidate for constructing phylogenies.

The only HERV left still active in the human genome is HERV-K. The rest are fragments and the longest one I have seen is around 7 thousand base pairs. You are talking about framents that are riddled with all kinds of mutations, making a genuine arguement for comon ancestry is hopelessly probablematic.

What does activity have to do with anything? Where are you going with this? All HERV's are heritable and are of viral origin. That is what makes them useful for phylogenetics. Are you saying that because HERV-W, for example, is no longer active that means it was never part of a viral genome? What exactly is your point, and where is the problem?

Because it still has an open reading frame, the rest are nearly extinct.

Because there are human-lineage specific insertions it tells us that the virus was active after the human-chimp split.

That would be where they got the H in front, brilliant deduction.

All ERV's found in humans have an H in front of them.

I can't wait for you to explain that one because it looks like something from left field to me.

HERV-W insertions are found in all primates but none of the insertions are specific to the human lineage. This means that all insertion events occured before the first split in the primate clade. If HERV-W were active after the human/chimp split then humans would have specific HERV-W insertions that other primates do not have.

What does an ERV with an open reading frame have to do with common ancestry? I don't know why you are jumping to conclusions but you have not even characterized the HERV-K virus.

All you need to know is that the sequence is viral in origin. If two individuals share a common insertion at an orthologous position this is strong evidence for common ancestry, just as shared ERV's between you and your siblings is best explained through heredity, not separate infections.

I have actually read the article a couple of times and if you notice the date it's 1999. This was before the Human Genome Project was complete which is why they can get away with these sweeping generalities.

What sweeping generalities. The sequences were published, as was mentioned in the Methods section:

"Primers were derived from the HERV-K18 published flanking sequence "

"Published RTVL-H sequences were used to query databases for RTVL-H loci with flanking sequences suitable for designing PCR primers. RTVL-Ha is an RTVL-H element spanning nucleotides 14602–20350 of cosmid clone N28H9 (accession no. Z71183)."

Sequences were known well before the final HGP sequence was made public. Do you really think that no one was sequencing DNA before the HGP was done?

Now if you think you have something in the way of evidence I will be glad to look at it but at this point you have some misconceptions, fundamental errors and misconceptions that you are using for an arguement.

I will ask again. You seem to duck this question every time. If individuals from different species share ERV insertions at orthologous positions in their genome, is this or is this not evidence for common ancestry? Please show your work.

Also, do you think all of the HERV's that you have are due to infections during your lifetime or did you inherit them from your parents? A very simple question that you continue to duck.

 

[rmwilliamsll]

and it is far from the absolute proof you think it is.

it bears constant repetition:
science does not do proof.
there is no such animal in science as absolute* proof, this is restricted to the domain of vodka and similiar liquors.

science does evidence, the strength of the evidence (like beyond reasonable doubt down to conjecture), the probability of the evidence standing up to scientific scrutiny and the consilience of this evidence to the overall frame of the science(how it fits and supports the structure).

notes:
* reference to absolut vodka and serious alcohols like everclear.
absolute alcohol is 100% or 200 proof.

 

[Chalnoth]

it bears constant repetition:
science does not do proof.
there is no such animal in science as absolute proof, this is restricted to the domain of vodka and similiar liquors.

And mathematics, don't forget that

When you're able to completely define the world in which you work, absolute proof is possible. Too bad we can't do that in science...we have this pesky 'reality' thing we have to deal with

 

[Loudmouth]

There is a great deal of uncertainty involved in using any of the transposable elements, particularly ERVs.

Uncertainty about what? Is anyone uncertain that they are heritable?

It doesn't work and it is far from the absolute proof you think it is.

Why doesn't it work?

Twice I elaborated at lenth on the current research being done and twice you completly ignored it. Now if you are going to talk in circles around the actual evidence then I will find something more productive to to with my time. What are your sources for making this sweeping statement and what is the evidence involved?

We have given you papers that outline the usefulness of ERV's for constructing phylogenies. You have handwaved them away for seemingly no reason.

Are you going to actually look at the source material or not because I am tired of having carefully prepared posts ignored. Look at the papers I have quoted, cited and linked and we can actually discuss the evidence involved.

The papers you have given us are not about shared ERV's at orthologous positions in the genome. ERV involvement in schizophrenia has nothing to do with the usefulness as a phylgentic marker.

[qutoe]They are not a reliable phyogentic marker and this line of arguement will be abandoned when it is realized.[/quote]

Again, why aren't they reliable?

Let's start here since you have yet to actually look at the ERVs themselves:

"Our examination of env dN/dS ratios in other HERV families suggests that the dominant role of reinfection and the persistence of a pool of active elements may be a general feature of HERV evolution. However, we note that one HERV family (HERV-L) does not encode an env gene, and that in another (HERV-H), >90% of the elements share large deletions in pol and env (30). Thus, in these cases (which are the two largest families in terms of copy number), proliferation has probably occurred via alternative mechanism(s) to reinfection. "

http://www.pnas.org/cgi/content/full/101/14/4894

And that alternative mechanism is recombination which is itself a viable phylogentic marker.

 

[mark kennedy]

And these LTR's are viral in origin and are heritable, which makes them a viable candidate for constructing phylogenies.

The LTRs are fragments of viruses that have been under purifying selection for 30 million years. The seqeunces are riddled with indels, substitutions, polymorphisms from one end to another. Until you actually compare two sequences in the respective genomes you have a lot of supposition and speculation.

What does activity have to do with anything? Where are you going with this?

First of all my comment about HERV-K ERVs being polymorphic was how they are characterized. That is something you have to do before you come to a conclusion or at least what scientists do before coming to a conclusion.

All HERV's are heritable and are of viral origin.

So 1% to 8% of the human genome is made up of viral fragments consisting primarily of LTR fragments? I don't think you realize what you are saying because you haven't had to actually study any of this.

That is what makes them useful for phylogenetics.

Fine, show me how it is used to establish taxonomic trees for other living systems. If it's so usefull then they must be using them to determine who the platypus is related to for instance. Show me how they are being used in the phylogentics of say, bacteria.

Are you saying that because HERV-W, for example, is no longer active that means it was never part of a viral genome?

I never said anything of the sort, I said only the HERV-K was active and the rest are nearly extinct. That simply characterizes them I never said whether or not they were part of a viral genome, whatever that is supposed to mean.

What exactly is your point, and where is the problem?

Transposable elements are notoriously unreliable for molecular clocks and constructing phylogenies. I know this, the scientists that study this know this and if you really look at it you will know this before it's over.

Because there are human-lineage specific insertions it tells us that the virus was active after the human-chimp split.

No, it tells us that it is polymorphic and has an open reading frame, that's all it tells us.

All ERV's found in humans have an H in front of them.

I gathered that but thanks for showing me you know that, it will become important later.

HERV-W insertions are found in all primates but none of the insertions are specific to the human lineage. This means that all insertion events occured before the first split in the primate clade. If HERV-W were active after the human/chimp split then humans would have specific HERV-W insertions that other primates do not have.

So you are saying that HERV-W insertions are found in every primate except humans, did I read that right. That is the first time I have seen an evolutionist admit something that is damaging to their position. This would mean that the split between all primate occured about 30 million years ago and only the human genome doesn't have it why exactly?

All you need to know is that the sequence is viral in origin.

No, that is not all you have to know, there is a great deal more to it then understanding what the V in ERV actually means.

If two individuals share a common insertion at an orthologous position this is strong evidence for common ancestry, just as shared ERV's between you and your siblings is best explained through heredity, not separate infections.

You keep saying that but you seem oblivious to the fact that 95% of the chimpanzee and human genome is the same. The odds of of any two sequences being being different are 1 in 5 and in the genes it is more like 1 in 100. It's not the simularities of the sequences that is important, it's the differences.

What sweeping generalities. The sequences were published, as was mentioned in the Methods section:

"Primers were derived from the HERV-K18 published flanking sequence "

"Published RTVL-H sequences were used to query databases for RTVL-H loci with flanking sequences suitable for designing PCR primers. RTVL-Ha is an RTVL-H element spanning nucleotides 14602–20350 of cosmid clone N28H9 (accession no. Z71183)."

Now you want to talk about primers, what is your interest in primers?

Sequences were known well before the final HGP sequence was made public. Do you really think that no one was sequencing DNA before the HGP was done?

They didn't have the entire sequence and after the publication of the HGP this nonesense of ERVs being somekind of a smoking gun for evolution stopped cold.

I will ask again. You seem to duck this question every time. If individuals from different species share ERV insertions at orthologous positions in their genome, is this or is this not evidence for common ancestry?

No, you are asking a syllogistic question, of course they share ERV fragments, the junk DNA lines up in 95% of the sequences across the board. I am far from convinced that 1% to 8% of the genomes is the framentary remains of viruses and you have not identified one orthologous position in the respective genomes.

Please show your work.

I have repeatedly, no one has read those posts and I am not spending hours preparing posts that are going to be ignored. Do your own work.

Also, do you think all of the HERV's that you have are due to infections during your lifetime or did you inherit them from your parents?

Unless they are actually a disfuntional part of the original genome then they are the result of germline invasions.

A very simple question that you continue to duck.

That is typical evolutionist rethoric, you talk in circles around the evidence and act as if I'm the one being evasive.

 

[rmwilliamsll]

So 1% to 8% of the human genome is made up of viral fragments consisting primarily of LTR fragments? I don't think you realize what you are saying because you haven't had to actually study any of this.


some numbers from one paper, they seem to agree pretty much with what i've read elsewhere.

from: http://jvi.asm.org/cgi/content/full/79/11/6997

Transposable elements (TEs) constitute a large fraction of the human genome (roughly 45% of the euchromatic component, and an indeterminately much larger amount of the heterochromatin), scattered over all chromosome regions with widely different repeat densities

or

The relative abundance of transposable elements (TEs) in eukaryotic genomes varies considerably among species. For example, it is estimated that 3% of the S. cerevisiae genome (Kim et al. 1998) and 6% of the C. elegans genome (C. elegans Sequencing Consortium 1998; Kidwell 2002) are composed of TEs, and up to 90% of the genomes of many higher eukaryotes are composed of TEs (e.g., Drosophila, 10% to 20% [Adams et al. 2000; Hoskins et al. 2002; Kaminker et al. 2002]; Arabidopsis, 10% [The Arabidopsis Genome Initiative 2000]; Mus, 37% [Smit 1999; Waterston et al. 2002]; Homo sapiens, 43% [Li et al. 2001]; Pinus, 90% [Flavell 1986; Pearce et al. 1996]).

from: http://mbe.oxfordjournals.org/cgi/content/full/20/11/1925

i've seen 1-8% for just HERV's.

 

[mark kennedy]

Uncertainty about what? Is anyone uncertain that they are heritable?

No, they are just uncertain if it's reliable.

Why doesn't it work?

For the same reason a roulette wheel would not give you a systematic pattern.

We have given you papers that outline the usefulness of ERV's for constructing phylogenies. You have handwaved them away for seemingly no reason.

I didn't handwave them off, you guys did. I did expostive posts of the primary source documents and you guys have completly ignored them. This has happened repeatedly and posting an abstract with a link is not an arguement, particularly when you ignore my discussion of the same article earlier in the thread.

The papers you have given us are not about shared ERV's at orthologous positions in the genome. ERV involvement in schizophrenia has nothing to do with the usefulness as a phylgentic marker.

No one is using them for genetic markers. Show me how they are being used in bacteria, show me how they are being used in fish, show me how they are being used period. In 1999 they proposed that ERVs could be used for taxonomic hiearchies but they never have been.

They are not a reliable phyogentic marker and this line of arguement will be abandoned when it is realized.

Again, why aren't they reliable?

Because they are not consistant, they are transposable elements and they don't change in a linear progression gradually accumulating differences. They are unreliable and you are dodging the actual evidence and I am getting tired of it.

And that alternative mechanism is recombination which is itself a viable phylogentic marker.

Recombination is a mechanism for eliminating viruses in the germline, how you consider this even remotely relevant is a mystery to me.

 

[Loudmouth]

The LTRs are fragments of viruses that have been under purifying selection for 30 million years.

Not all ERV's have been under purifying selection for 30 million years. That's the whole point.

The seqeunces are riddled with indels, substitutions, polymorphisms from one end to another. Until you actually compare two sequences in the respective genomes you have a lot of supposition and speculation.

The paper I linked to earlier did compare them, and the comparison yielded a phylogenetic tree that agreed with insertion time and phylogenetic trees derived from morphology. It isn't speculation or supposition.

First of all my comment about HERV-K ERVs being polymorphic was how they are characterized. That is something you have to do before you come to a conclusion or at least what scientists do before coming to a conclusion.

And the polymorphic ERV's are not found in other primates. That is consistent with an insertion event in the human lineage after the human-chimp split.

So 1% to 8% of the human genome is made up of viral fragments consisting primarily of LTR fragments? I don't think you realize what you are saying because you haven't had to actually study any of this.

Yes. 1-8% of our genome is viral insertions, either through primary infection, recombination, or transposition.

Fine, show me how it is used to establish taxonomic trees for other living systems. If it's so usefull then they must be using them to determine who the platypus is related to for instance. Show me how they are being used in the phylogentics of say, bacteria.

There is too much horizontal gene transfer in bacteria. However, ERV's have been used to construct phylogenies in cats, ungulates (linked whales to ungulates), and sheep to name a few. I can get the references if you like, but I remember giving them to you before with no reply.

I never said anything of the sort, I said only the HERV-K was active and the rest are nearly extinct. That simply characterizes them I never said whether or not they were part of a viral genome, whatever that is supposed to mean.

These HERV's are hereditary and viral in origin, which makes them a viable phylogenetic marker.

Transposable elements are notoriously unreliable for molecular clocks and constructing phylogenies. I know this, the scientists that study this know this and if you really look at it you will know this before it's over.

And yet the scientists are using them for just that. The insertion events are anything but unreliable.

So you are saying that HERV-W insertions are found in every primate except humans, did I read that right. That is the first time I have seen an evolutionist admit something that is damaging to their position. This would mean that the split between all primate occured about 30 million years ago and only the human genome doesn't have it why exactly?

It's been a while since I looked at HERV-W insertions. You would expect human specific transpositions. What I am saying is that there are no human specific insertions. What insertions we do have are shared by other primates, as is consistent with common ancestry for all primates.

No, that is not all you have to know, there is a great deal more to it then understanding what the V in ERV actually means.

Then what more is there to it?

You keep saying that but you seem oblivious to the fact that 95% of the chimpanzee and human genome is the same. The odds of of any two sequences being being different are 1 in 5 and in the genes it is more like 1 in 100. It's not the simularities of the sequences that is important, it's the differences.

But there is little doubt that the two sequences, even if they differ by 5%, are from the same viral insertion event.

Now you want to talk about primers, what is your interest in primers?

The viral sequence and flanking DNA was already known. This is how they knew they were orthologous.

They didn't have the entire sequence and after the publication of the HGP this nonesense of ERVs being somekind of a smoking gun for evolution stopped cold.

You don't need to know the whole sequence to know that two ERV's are in the same orthologous position in two different species.

No, you are asking a syllogistic question, of course they share ERV fragments, the junk DNA lines up in 95% of the sequences across the board. I am far from convinced that 1% to 8% of the genomes is the framentary remains of viruses and you have not identified one orthologous position in the respective genomes.

If I show that these ERV's are at orthologous positions will you concede that this is strong evidence of common ancestry? I am not going to do the work if you are going to dismiss it outright.

I have repeatedly, no one has read those posts and I am not spending hours preparing posts that are going to be ignored. Do your own work.

Your posts show that you don't understand the importance of the placement of the ERV's, which is whole reason that they are useful for constructing phylogenies.

Unless they are actually a disfuntional part of the original genome then they are the result of germline invasions.

When did these germline invasions occur? In your parents, or further back?

That is typical evolutionist rethoric, you talk in circles around the evidence and act as if I'm the one being evasive.

You have been evasive this entire thread. We keep talking about orthologous ERV's and you do everything to shift the focus to non-orthologous ERV's.

 

[Loudmouth]

For the same reason a roulette wheel would not give you a systematic pattern.

That's why ERV's work, because the odds of two individuals sharing the same ERV insertions at orthologous positions through separate infection events is highly improbable.

I didn't handwave them off, you guys did. I did expostive posts of the primary source documents and you guys have completly ignored them.

I didn't ignore them. They had nothing to do with orthologous ERV's between species.

No one is using them for genetic markers.

Baloney. I have already linked to a paper that does just that. I don't understand why you continue to deny it.

In 1999 they proposed that ERVs could be used for taxonomic hiearchies but they never have been.

They didn't suggest it. They did it.

Because they are not consistant, they are transposable elements and they don't change in a linear progression gradually accumulating differences. They are unreliable and you are dodging the actual evidence and I am getting tired of it.

Transposable elements do not insert at the same position in the genome every time. They insert randomly. Therefore, the chances of separate transposition events creating the same insertion are nil, especially when dozens of insertions are considered.

Recombination is a mechanism for eliminating viruses in the germline, how you consider this even remotely relevant is a mystery to me.

Recombination is what changes ERV sequences, and tracking those changes through phylogenies is what adds weight to the analysis.

 

[dad]

Retroviruses insert randomly into the genome among thousands of possible insertion sites. Let's say that there are 5,000 possible insertion sites for a virus, a very conservative number. That would mean that the chances of two individuals sharing the same insertion is 1 in 5,000. In the case of primates, there are dozens and dozens of shared insertions. The chances of sharing 20 insertions, by separate chance infections, is 1 in 5,000^20, or 1 in 9.53674316 × 10^73


....

Before looking at anything else, you say in the case of primates many insertions are shared. In other words, the monkey family, and apes, etc.
I can see two possibilities there. Some primate kinds were taken on the ark, and were affected by pre flood wickedness of mankind. After the flood, for a century where fast adaptions were possible, more species developed. Traces of the insertions were therefore all through the primate grouping. And, of course, in man.

The other idea is that the different past meant that insertions did not at all work the way they do now.

 

[shernren]

Fine, show me how it is used to establish taxonomic trees for other living systems. If it's so usefull then they must be using them to determine who the platypus is related to for instance. Show me how they are being used in the phylogentics of say, bacteria.

It's called Google. Searching for "ERV phylogeny" yielded

result #6: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=524511

Characterization of an endogenous retrovirus class in elephants and their relatives

Here we examine whether proviral-like sequences may be suitable molecular probes for investigating the phylogeny of groups known to have high element diversity. As a test we characterized ERV-Ls occurring in a sample of extant members of superorder Uranotheria (Asian and African elephants, manatees, and hyraxes). The ERV-L complement in this group is even more diverse than previously suspected, and there is sequence evidence for active expansion, particularly in elephantids. Many of the elements characterized have protein coding potential suggestive of activity. In general, the evidence supports the hypothesis that the complement had a single origin within basal Uranotheria.

Even when merely ERV-like elements (ERV-L) are used instead of actual ERVs the methodology still yields phylogenetic data.

result #13:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=114757

Identification, Phylogeny, and Evolution of Retroviral Elements Based on Their Envelope Genes

[Discussion] Accordingly, the present study already provides a catalog of human sequences and a method for updating and extending the search to other genomes when they are entirely sequenced. In the case of the mouse genome, for instance, we have already detected two new mouse ERV sequences. One of them, MuERV-U1, is likely to be mouse specific, while the second (AC020617) is homologous to the human HERV-F(c) family. The latter case is reminiscent of the HERV-L family, which is shared by all mammalian species and most probably corresponds to an ancestral retroelement already present in living species before the mammalian radiation and which therefore constitutes an evolution marker among mammals (4).

If you were so confident there weren't any why didn't you bother to search?

Transposable elements are notoriously unreliable for molecular clocks and constructing phylogenies. I know this, the scientists that study this know this and if you really look at it you will know this before it's over.

Molecular clocks, yes. Phylogenies, source please.

They didn't have the entire sequence and after the publication of the HGP this nonesense of ERVs being somekind of a smoking gun for evolution stopped cold.

Researchers disagree:

Human endogenous retrovirus sequences (HERVs), which have become trapped as Mendelian genes and fixed in the germ line (9), constitute 7 to 8% of the human genome (8, 26). The sequencing of the human (Homo sapiens) genome (26) and the draft sequence of the chimpanzee (Pan troglodytes) genome (16) have facilitated the evolutionary studies of ERVs and related sequences. The Homo-Pan speciation has been estimated to have occurred between 4.6 and 6.2 million years ago (15). The genomic nonidentity is approximately 1.2% (15, 17) up to 5% (14), depending on analysis methods.

a paper you yourself first brought up in your ERV thread: http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=1346942

 

[Loudmouth]

Before looking at anything else, you say in the case of primates many insertions are shared. In other words, the monkey family, and apes, etc.
I can see two possibilities there. Some primate kinds were taken on the ark, and were affected by pre flood wickedness of mankind. After the flood, for a century where fast adaptions were possible, more species developed. Traces of the insertions were therefore all through the primate grouping. And, of course, in man.

That doesn't explain the nested hierarchy.

The other idea is that the different past meant that insertions did not at all work the way they do now.

Fantasies do not trump factual observations.

 

[Schroeder]

Well, I'll explain it in greater detail. When a virus infects a cell it injects its own RNA into the cell. This RNA rewrites the genetic code of the cell and causes the cell to manufacture more of the virus until it bursts and releases the copies.

What we are referring to is a particular rare occurance of this process. What happens is, a virus attempts to infect a sex cell(sperm or egg). The virus manages to rewrite (or add) a small portion to the cells DNA. Then that particular cell happens to fertilize or be fertilized. That creature then makes it to maturity and has offspring, passing on the viral imprint in that specific part of the DNA strand. Offspring from then on bear that retro-viral imprint (unless that portion is deleted). The chances of this happening in the same place in the genetic code with the same virus of even two individuals is astronomical, nevermind across multiple individuals.

We can therefore reasonably conclude that any individuals with the same retro-viral imprint in the same place are related. It just so happens that the entire human and chimp population share such a mark. There are more as well, there is a heirarchy that reflects our taxamonic structure. Those are two pieces of independently coorborating evidence.

i find it odd that you will not accept the odds given for it to happen in the same place in the gentic code ect ect. but will accept them for some of the odds given on your side of the arguement. as i have been told it only has to happen once no matter what the odds are. this fits for your side not the other. how telling.

 

[caravelair]

i find it odd that you will not accept the odds given for it to happen in the same place in the gentic code ect ect. but will accept them for some of the odds given on your side of the arguement. as i have been told it only has to happen once no matter what the odds are. this fits for your side not the other. how telling.

you're really going to have to elaborate if you want people to know what you're talking about.

 

[Chalnoth]

i find it odd that you will not accept the odds given for it to happen in the same place in the gentic code ect ect. but will accept them for some of the odds given on your side of the arguement. as i have been told it only has to happen once no matter what the odds are. this fits for your side not the other. how telling.

Whenever you find an object or observation that appears in such a way that it could not have arisen randomly, that is a sign of some sort of process behind that object or observation. Once you find the right process, the unlikely suddenly becomes expected.

Here we have a series of markers that are inherited from parent to child, and exist between species only in a strict hierarchy consistent with the phylogenic tree. The obvious process through which such a thing could become expected is that this is a family tree.

Now, I'm going to assume that you were talking about abiogenesis here, and the probability of abiogenesis calculations. Here again, what we should do is find a process through which abiogenesis can occur, not say that it couldn't. Scientists have done this, and there are currently a large number of abiogenesis theories that are highly plausible. We don't yet know which of them, if any, is correct, but perhaps one day we'll be able to obtain experimental evidence that supports one or the other.

 

[Loudmouth]

i find it odd that you will not accept the odds given for it to happen in the same place in the gentic code ect ect. but will accept them for some of the odds given on your side of the arguement. as i have been told it only has to happen once no matter what the odds are. this fits for your side not the other. how telling.

There is another observed mechanism, common ancestry, that is much more likely given the odds. For example, it is not that stunning that the thousands of HERV's that you and your siblings share are also found in your parents at the same spot in their genomes. The odds of you sharing the same HERV's with your siblings is nearly 1 in 1. This is because of common ancestry. The same mechanism is then applied to individuals from different species. So what do you think scientists should go with, 1 in a trillion trillion odds or the nearly 1 in 1 odds?

 

[sfs]

ERVs provide support for common descent in two ways. First, specific instances of the same ERV, at the same spot in the genome, are found in clusters of species. Consistently, the species that share specific ERVs are species that (according to conventional science) share a common ancestor, while more distantly related species lack the ERV; this suggests that the ERV was present in a species that was ancestral to the cluster and not to others, which provides strong support for the evolutionary picture of species diversity.

Second, whole families of ERV also mirror the phylogenetic tree as described by evolutionary biology. ERV families that are old (as measured by the number of mutations that they have accumulated) are shared by many diverse species, while ERV families that are young are shared only by small groups of closely related species.

As far as I can tell, none of Mark's responses undercuts this evidence. His reasons for ignoring ERVs include the following:

ERVs are too short to be useful for phylogeny
ERVs are hundreds to thousands of base pairs long. That is plenty of sequence for identifying the type of ERV, especially for more recent families. (And where it isn't, the ERV is simply uninformative. Those aren't the ones being used for inferring or supporting phylogeny.) I don't know where Mark got this idea -- perhaps from misunderstanding a statement in the PNAS article he likes to quote (which was talking about how short the reverse transcription primer sequence is) -- but it's wrong.

The problem with ERVs as a tool for doing phylogeny is not that they're inaccurate, but that they're highly inefficient. They represent a single character, which a species either has or does not have. That means you need to study many ERVs to reconstruct a phylogeny. A single gene, by contrast, will provide many characters (many mutations) for distinguishing different branches of a tree.

ERV taxonomy is confused
This is irrelevant. Scientists disagree about exactly how to classify ERVs, but have no difficulty in identifying ERVs that belong to the same family.

ERV naming is inconsistent
Uh, yeah. So what?

ERVs have accumulated lots of substitutions, inversions, deletions and whatnots.
Sure, ERVs will eventually accumulate enough mutations to be unrecognizable. Note that Mark makes no attempt to quantify how long this takes. In reality, ERVs are easily identifiable for at least several tens of millions of years, and usable for hundreds of millions of years. (Any ERV that is not recognizable is, again, not informative.)

Real Scientists stopped paying any attention to ERVs after the Human Genome Project
As far as I can tell, Mark simply made this one up. The PNAS article that he likes, which was written well after the HGP, notes that ERVs are useful for constructing phylogenies. I don't know if he skipped over that sentence, or if he includes the authors (of a review article!) among those benighted souls who haven't read the research literature the way he has.

ERVs are transposons
This is another "so what?" one. Yes, most ERVs that we see can transpose, which just means that they can copy themselves into a new spot in the genome (while still leaving a copy in their original location). Each insertion of a copy of the ERV, whether it is the original insertion from an infectious virus, or a later transposition to a new spot in the genome, is a unique and irreversible evolutionary event. That means they are ideal features for reconstructing phylogenies. Perhaps I missed it, but I haven't seen Mark offer any explanation of why he thinks being a transposon disqualifies the ERV for this purpose, so I can't offer a more detailed response.

As far as I can see, ERVs still offer strong and detailed support for common ancestry in a variety of taxa.

 

[dad]

That doesn't explain the nested hierarchy.

Meaning what, exactly? Of primates? What is it that it doesn't explain? If wicked pre flood humans infected various primates, and they adapted into other species, etc etc, you really are not saying anything here.

Fantasies do not trump factual observations

True, and what do we observe that is not fantasy here, exactly? Virus infected much of the primate species, and man in the past?

 

[Cre8]

why do the creationists never have anything to say about these things?

Because creationists are without retort.

www.aninfidelmanifesto.com

 

[shernren]

ERVs are transposons
This is another "so what?" one. Yes, most ERVs that we see can transpose, which just means that they can copy themselves into a new spot in the genome (while still leaving a copy in their original location). Each insertion of a copy of the ERV, whether it is the original insertion from an infectious virus, or a later transposition to a new spot in the genome, is a unique and irreversible evolutionary event. That means they are ideal features for reconstructing phylogenies. Perhaps I missed it, but I haven't seen Mark offer any explanation of why he thinks being a transposon disqualifies the ERV for this purpose, so I can't offer a more detailed response.

As far as I can see, ERVs still offer strong and detailed support for common ancestry in a variety of taxa.

I'm still confused about something, when precisely in a cell's life cycle does this "transposition" occur? And is transposition a rare or common process? Does it happen on an organismal or populational level? (Does that last question actually have any useful answer or does it show that I've misunderstood something?)

Devil's advocate:
But if you acknowledge that ERVs are transposable, doesn't that detract credibility from your having ostensibly identified them at the same loci?

Say you claim that ERV-X was found in both chimps and humans at locus A, and that this proves a common origin. But ERV-X might exist at another locus B in the human genome. I claim that God originally created the chimp with ERV-X at locus A in chimps and at locus B in humans, over time ERV-X transposed over to locus A and that's how your ostensible "connection" came about, by a fluke transposition. Who's to say that I'm wrong and you're right?