Chimpanzee Genome

[sfs]

I have presented accurate facts throughout. I have referred to the same table from the very start of this thread. That table has not changed.

That table also appears to be the source for all later statements of the fraction of ERVs in the human genome, which can be variously reported as 4.6%, 5-8% or "up to 8%". This is all really straight-forward.

 

[Loudmouth]

That's really all that has kept my interest. Over time I discovered a remarkable thing, these apologists for Darwinism can't get their facts straight.

That's rich.

Table 11. Human genome paper. Look at it.

Table 2. Chimp genome paper. Notice that the insertions are "LINEAGE SPECIFIC".

Polavarapu et al. (2006), only looked at 425 insertions out of the hundreds of thousands in the chimp genome.

When are you going to get these facts straight?

 

[mark kennedy]

And there we have it. Science-dilettantes like Mark think that scientists take a casual look at various brain specimens and decide which "look pretty close to me."

When one has zero familiarity with the evidence for evolution and common descent, that makes it a whole easier to dismiss the science. (Ignorance it not only bliss. It simplifies decision-making immensely!)

It also makes it easier to strut about declaring oneself the victor and to look down on all of those deluded scientists and their meaningless Ph.D. degrees!

Which is specifically pertaining to what 'fact' in evidence exactly? I'm not dismissing anything, I'm telling you what the evidence for the Taung Child is telling you, it's a Chimpanzee.

 

[NoPostDocFrock]

Yes, you are still ignoring the facts.

That is his modus operandi.

 

[mark kennedy]

I don't know about anyone else, but I don't see a problem here.

The human genome is littered by endogenous retrovirus sequences (HERVs), which constitute up to 8% of the total genomic sequence...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 Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes​

Retroelements and the human genome: New perspectives on an old relation

I wouldn't give it a second thought if not for the fact that these homology arguments are based on the appearance that the two genomes are virtually identical. I've run into this again and again with regards to the overall divergence. The two genomes diverge by 5% at least but the popular press continually tells us that we are 98% the same in our DNA, which is true, unless you count the indels.

The conclusion is the old saw that we share 98.5% of our DNA sequence with chimpanzee is probably in error. For this sample, a better estimate would be that 95% of the base pairs are exactly shared between chimpanzee and human DNA. In this sample of 779 kb, the divergence due to base substitution is 1.4%, and there is an additional 3.4% difference due to the presence of indels (Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels)​

I still wouldn't have a problem if not for the incessant claims that I'm in error. I'll get a flurry of posters who tell me I've been proven wrong or that I can't get my facts straight and yet none of you want to admit to the straightforward facts as they are clearly explained in the scientific literature.

I run into this every single time I try to discuss genomics on here. LM makes an argument based on an old Talk Origins argument saying ERVS are 1% of the Human Genome.

In humans, endogenous retroviruses occupy about 1% of the genome, in total constituting ~30,000 different retroviruses embedded in each person's genomic DNA (Sverdlov 2000) Prediction 4.5: Molecular evidence - Endogenous retroviruses.​

He eventually comes up with 4% based on the table in the Human Genome paper but the latest evidence I can find is that it's 8% of the Human genome overall. What is more those ERVs account for 7% of the divergence due to indels. He want's to argue that the ERVs in the respective genomes are 'virtually identical' which is odd given this:

According to this table, the chimp genome has 234 ERV class 1 elements not found in the human genome, and they total more than 1 million base pairs of sequence.

That's over a million base pairs of sequence that become a permanent part of the Chimpanzee genome as the result of germline invasions after the split. You really don't see a problem? Even thought the PtERV2 sequences are not as big,' the reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.'.

There are obvious problems here that probably don't effect the overall homology argument much at all. It's simple enough, just make some adjustments in the overall percentages.

If all 234 were full length, and they run about 7 kb per repeat, that would be 1.6 million base pairs. That's 2% of the total contribution of ERV class 1 elements to the human or chimp genome. (234 is a much smaller fraction of the total number of ERVs in the genome, but that's not surprising: the recent, lineage-specific insertions are much more likely to still be full length, and therefore much longer than the typical ERV fossil, which just consists of the terminal repeat portion.)

Thank you! So what you are saying is that the divergent Class 1 ERVs make up 1.6 Mbps, a total of 2% in the respective genomes. I promise you I'm not trying to be pedantic here, I just want to clarify that this is a reliable statistic as an overall percentage.

So what was the problem again? And what does this have to do with the evidence that ERV insertion points were inherited?

Probably none really, I can make my standard arguments that the divergence is too great and the evolutionists can simple defend the view that their not. I really don't have a problem with that, it's what I would expect. If your convinced by the evidence of common ancestry that's fine. I would just like the facts used as evidence to be established without vacillating by millions of base pairs.

You've always been helpful with this sort of thing Steve. The debates often get heated which is part of the whole controversy between Creationism and Evolution anyway. I would appreciate just a little clarification on what the divergence actually is before I start fielding these incessant personal attacks.

That table also appears to be the source for all later statements of the fraction of ERVs in the human genome, which can be variously reported as 4.6%, 5-8% or "up to 8%". This is all really straight-forward.

That's not really all that straightforward. I fully appreciate that you might be looking at different things using different methods. Things are constantly being updated and revised so for the Human Genome paper to say ERVs make up 4.6% of the Human Genome and a report years later says that it's 8% it just means the estimate has been adjusted. If we are talking about less then 2% divergence overall it's not that big of a deal to explain it.

That's not what is going on here. Before the facts are established I'm getting these petty personal remarks about how I'm making glaring mistakes, lying about the facts and it's all just a figment of my 'perverse imagination'. Then when LM makes glaring errors he gets a pass. Hardly sounds objective to me.

Grace and peace,
Mark

 

[Tomk80]

Which is specifically pertaining to what 'fact' in evidence exactly? I'm not dismissing anything, I'm telling you what the evidence for the Taung Child is telling you, it's a Chimpanzee.

And the experts who actually know what they are talking about disagree with you. The article you linked to was clear on that.

Furthermore, the differences between the skull of the Taung child and a chimpanzee skull are obvious. Enlarged incisors and eyebrow ridge in the chimpanzee but not the Taung child, weaker jawline for the Taung child compared to the chimp. The Taung child is most definitely not a chimp.

 

[Loudmouth]

I wouldn't give it a second thought if not for the fact that these homology arguments are based on the appearance that the two genomes are virtually identical.

Of the 200,000 ERV's found in humans only 100 of those are not found in chimps. That seems pretty identical to me.

The two genomes diverge by 5% at least but the popular press continually tells us that we are 98% the same in our DNA, which is true, unless you count the indels.

And? Why is this a problem? Are you saying that evolution should not produce changes over time?

I still wouldn't have a problem if not for the incessant claims that I'm in error. I'll get a flurry of posters who tell me I've been proven wrong or that I can't get my facts straight and yet none of you want to admit to the straightforward facts as they are clearly explained in the scientific literature.

You are ignoring what is clearly explained, such as the fact that Polavarapu et al. (2006) only looked at 425 chimp ERV's when there are hundreds of thousands of ERV's in the chimp genome. Why do you always fail to mention this?

I run into this every single time I try to discuss genomics on here. LM makes an argument based on an old Talk Origins argument saying ERVS are 1% of the Human Genome.

Why are you still hung up on this? Really? That was an early estimate based on incomplete genomic data. The complete story is given in the human genome paper.

He eventually comes up with 4% based on the table in the Human Genome paper but the latest evidence I can find is that it's 8% of the Human genome overall.

You are once again confusing the facts. I have explained this over and over and over. The 4% excludes MaLR's. The 8% includes them.

What is more those ERVs account for 7% of the divergence due to indels.

And why is that a problem?

He want's to argue that the ERVs in the respective genomes are 'virtually identical'

99.9% of human ERV's are found at orthologous positions in the chimp genome.

That's over a million base pairs of sequence that become a permanent part of the Chimpanzee genome as the result of germline invasions after the split. You really don't see a problem?

No, I really don't see the problem. What is the problem? Spell it out for me.

Even thought the PtERV2 sequences are not as big,' the reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.'.

Right, so the divergence did not occur in the ape genomes. It occurred in the virus itself. The retrovirus was evolving rapidly during this time which explains the difference between PtERV insertions, all of which are non-orthologous between ape species which indicates independent insertions. I have already explained this as well. Why do I have to keep repeating myself?

Thank you! So what you are saying is that the divergent Class 1 ERVs make up 1.6 Mbps, a total of 2% in the respective genomes.

Your math is getting really bad. 1.6 million bases is 0.2% of a 3 billion base genome.

If your convinced by the evidence of common ancestry that's fine. I would just like the facts used as evidence to be established without vacillating by millions of base pairs.

Another irony meter explodes.

Things are constantly being updated and revised so for the Human Genome paper to say ERVs make up 4.6% of the Human Genome and a report years later says that it's 8% it just means the estimate has been adjusted.

The estimate is the same. I have been over this multiple times as well. The chart you are using is from a review paper. There is no new estimate. The author is just lumping MaLR's in with the ERV classes. That's it. That is the only difference.

Do you understand the difference between a review paper and a primary paper?

That's not what is going on here. Before the facts are established I'm getting these petty personal remarks about how I'm making glaring mistakes, lying about the facts and it's all just a figment of my 'perverse imagination'. Then when LM makes glaring errors he gets a pass. Hardly sounds objective to me.

What glaring errors am I making in this thread? Cite one. Just one.

 

[sfs]

The human genome is littered by endogenous retrovirus sequences (HERVs), which constitute up to 8% of the total genomic sequence...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 Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes​

Retroelements and the human genome: New perspectives on an old relation

All the sources you cite agree that LTRs constitute about 8% of the human genome. All point back as their ultimate source to the human genome sequencing paper; if you can find an independent later estimate, I'd like to see it. The only substantial difference between the breakdowns is that the human genome paper assigned 4.6% of the genome to ERVs and 3.6% to MaLR, while in the above table the MaLR's seem to have been absorbed into ERV class 3. What difference does any of this make?

I wouldn't give it a second thought if not for the fact that these homology arguments are based on the appearance that the two genomes are virtually identical.

Completely wrong. The homology arguments are based on the presence of specific ERV insertion sites; those sites form a nested hierarchy when you compare species. To buttress this, the degree to which ERV insertion sites are shared across species matches extremely well how old the ERV insertions are, based on the number of mutations in their terminal repeats.

Are you ever going to deal with the real argument, rather than all of this other stuff?

I run into this every single time I try to discuss genomics on here. LM makes an argument based on an old Talk Origins argument saying ERVS are 1% of the Human Genome.

I'm only dealing with the argument you're presenting here. Whether someone else has presented a different wrong argument somewhere else has nothing to do with it.

He eventually comes up with 4% based on the table in the Human Genome paper but the latest evidence I can find is that it's 8% of the Human genome overall.

The only evidence you've presented here suggests that the only difference between 4% (5%, actually, since the number was 4.6%) and 8% is what exactly is being counted as an ERV. Mind you, if estimates of the fraction really did range between 4% and 8% it wouldn't be particularly interesting, but all of these numbers seem to be based on a single study.

What is more those ERVs account for 7% of the divergence due to indels. He want's to argue that the ERVs in the respective genomes are 'virtually identical' which is odd given this:


That's over a million base pairs of sequence that become a permanent part of the Chimpanzee genome as the result of germline invasions after the split. You really don't see a problem?

No, I really, really don't see a problem. That's why I said I didn't see a problem. That's why I asked you what the problem is. Are you going to reveal the problem soon? So far everything you've said seems to be perfectly consistent with standard evolutionary accounts.

Even thought the PtERV2 sequences are not as big,' the reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.'.

Very likely indicating that the divergence between the subfamilies didn't arise by mutation since divergence between human and chimp, as you've already been told. Again, what's the problem?

There are obvious problems here that probably don't effect the overall homology argument much at all. It's simple enough, just make some adjustments in the overall percentages.

The problems are obvious only to you. What the heck is your point?

Thank you! So what you are saying is that the divergent Class 1 ERVs make up 1.6 Mbps, a total of 2% in the respective genomes. I promise you I'm not trying to be pedantic here, I just want to clarify that this is a reliable statistic as an overall percentage.

A total of 2% of the ERV sequence in the genomes.

Probably none really, I can make my standard arguments that the divergence is too great and the evolutionists can simple defend the view that their not. I really don't have a problem with that, it's what I would expect. If your convinced by the evidence of common ancestry that's fine. I would just like the facts used as evidence to be established without vacillating by millions of base pairs.

You've always been helpful with this sort of thing Steve. The debates often get heated which is part of the whole controversy between Creationism and Evolution anyway. I would appreciate just a little clarification on what the divergence actually is before I start fielding these incessant personal attacks.

That's not really all that straightforward. I fully appreciate that you might be looking at different things using different methods. Things are constantly being updated and revised so for the Human Genome paper to say ERVs make up 4.6% of the Human Genome and a report years later says that it's 8% it just means the estimate has been adjusted. If we are talking about less then 2% divergence overall it's not that big of a deal to explain it.

That's not what is going on here. Before the facts are established I'm getting these petty personal remarks about how I'm making glaring mistakes, lying about the facts and it's all just a figment of my 'perverse imagination'. Then when LM makes glaring errors he gets a pass. Hardly sounds objective to me.

You introduced this subject by saying you were refuting the argument for common descent from ERVs. You haven't refuted anything here. The only thing you've pointed out is that some LTRs can be classified in different ways and so show up in different lines of summary charts.

 

[Notedstrangeperson]

(Don't mind me butting in again )

Taung is and was a Chimpanzee ancestor, I think that would at least be a possibility if it were permissible to suggest that in the Darwinian theater of the mind.
...
I'm not dismissing anything, I'm telling you what the evidence for the Taung Child is telling you, it's a Chimpanzee.

Tomk80 has already mentioned Dr. Dart's reasoning on why they think the Taung child is a human ancestor rather than just an ape (as well as other anatomical differences such as the size of the incisors), but I'd like to add more.

The Taung Child - an infant specimen of Australopithecus Africanus - still has a partly-open metopic suture: a thin band of cartilage that separates the two frontal bones in the skull, and is responsible (along with other sutures) for giving the child a fontanelle or "soft spot". In infant chimps is closes shortly after their first teeth emerge, whereas in humans (because the brain continues to grow greatly after birth) it remains munch longer.

The Taung Child was estimated to have been around 3 or 4 years old when it died. If it was a chimpanzee the metopic suture would have been fused by this time. The fact that it still had a partly-open suture long after birth suggested a more human-like pattern of brain growth.

The type specimen for Australopithecus africanus (Taung) includes a natural endocast that reproduces most of the external morphology of the right cerebral hemisphere and a fragment of fossilized face that articulates with the endocast. Despite the fact that Taung died between 3 and 4 y of age, the endocast reproduces a small triangular-shaped remnant of the anterior fontanelle, from which a clear metopic suture (MS) courses rostrally along the midline ... In great apes, the MS normally fuses shortly after birth, such that unfused MS similar to Taung’s are rare. In humans, however, MS fuses well after birth, and partially or unfused MS are frequent. In gracile fossil adult hominins that lived between 3.0 and 1.5 million years ago, MS are also relatively frequent, indicating that the modern human-like pattern of late MS fusion may have become adaptive during early hominin evolution.​

Metopic suture of Taung - pnas.org​

​

 

[Loudmouth]

Even thought the PtERV2 sequences are not as big,' the reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human.'.

This quote mine deserves its own post. Do you understand what that section of the paper is saying, Mark? Why don't we see what the ENTIRE sentence actually says (which you so often have to do with creationist quote mines):

"The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human. "

I highlighted the important part for you. What do you think this means, Mark? It means that the virus was evolving very quickly outside of its host. This accounts for the divergence as the paper clearly states.

 

[sfs]

This quote mine deserves its own post. Do you understand what that section of
I highlighted the important part for you. What do you think this means, Mark? It means that the virus was evolving very quickly outside of its host. This accounts for the divergence as the paper clearly states.

Indeed, one of the notable features of retroviruses is that they mutate very fast when replicating as viruses.

 

[NoPostDocFrock]

Before the facts are established I'm getting these petty personal remarks about how I'm making glaring mistakes, lying about the facts and it's all just a figment of my 'perverse imagination'.​

Hmm. I wonder why?​

 

[mark kennedy]

So says the person who doesn't understand the difference between shared and lineage specific insertions.

Don't understand? My whole argument is based on the divergence which is by definition 'lineage specific' in the respective genomes.

False. That is NOT what either paper says. First, the 234 ERV class I insertions are not all of the insertions in the chimp genome. Those are the lineage specific insertions found in chimps. You keep leaving this fact out. Also, the "PtERV1 is one of the most abundant families" is based on a survey of just 0.2% of the total ERV's in the chimp genome. You keep ignoring this fact as well.

According to Steve,

According to this table, the chimp genome has 234 ERV class 1 elements not found in the human genome, and they total more than 1 million base pairs of sequence...That's 2% of the total contribution of ERV class 1 elements to the human or chimp genome.

That's pretty abundant don't you think?

Yes. It is a question of how each chart incorporates MaLR's which have features of both ERV LTR's and retrotransposons. If I understand it correctly, the LTR from an ERV has hitched a ride on a transposon so the insertions themselves are not retroviral driven but transposon driven. At the same time, they do contain viral DNA in the form of LTR's. It all depends on how you want to count MaLR's. For clarity, I prefer to focus just on the insertions that are driven by retroviral insertion which would be the 3 classes listed in the Table 11 of the human genome paper.

Ok LM, I was never all that concerned with what we actually looked at with regard to the ERVs. I wanted to be sure of the proportion of the various sequences and Steve came through for us again, hopefully we can start to focus on categories and functions now.

I have presented accurate facts throughout. I have referred to the same table from the very start of this thread. That table has not changed.

You have one table from a paper that is over ten years old, that doesn't make it wrong, that just means there are a lot of other things to look at as well. The fact is that you can't be trusted to get the facts straight, you never have been. I think your capable of it but you keep getting this tunnel vision that it's some kind of a smoking gun for common ancestry, it's not. For us to share a lot of DNA with Chimpanzees really prove very little, makes a nice homology argument but that's about it. What you need is a molecular basis for adaptive evolution. You seem to forget, we have a brain three times bigger then a chimp.

Again, your reading comprehension is getting in your way. It all has to do with the MaLR's. MaLR's do have ERV sequences, but they were not created by the insertion of a retrovirus into the genome. Rather, they were produced by transposon activity. Instead of having to discuss two different mechanisms of insertion I wanted to focus on just one, the mechanism that retroviruses use to insert their genome into the host genome. For that purpose, I have focused on the 200,000 insertions spread over ERV's I-III in table 11 of the human genome paper.

It matters little to me which ones we look at. My interest is where they are, the size of the sequences, what they actually do and whether or not this has anything to do with common ancestry.

So it demolishes your entire argument.

I haven't really made an argument yet.

So how did they determine which HERV-K insertions were lineage specific and which were shared? Please, humor me.

We can get to that but I'm tracking down the current research on the subject. As it always happens once I get into one of these debates I get busy.

 

[mark kennedy]

All the sources you cite agree that LTRs constitute about 8% of the human genome. All point back as their ultimate source to the human genome sequencing paper; if you can find an independent later estimate, I'd like to see it. The only substantial difference between the breakdowns is that the human genome paper assigned 4.6% of the genome to ERVs and 3.6% to MaLR, while in the above table the MaLR's seem to have been absorbed into ERV class 3. What difference does any of this make?

It doesn't make a lot of difference, never thought it did. It just looks like a really bad homology argument. The discussion was on ERVs, I was just wanting to establish, as a percentage, what the size of the ERVs were in the respective genomes. It's 8%, that's all I really wanted. Now your telling me that nothing has really changed proportionally since the Human Genome paper was published, they are just categorized differently from time to time. That's not unreasonable, it's really all I needed.

Completely wrong. The homology arguments are based on the presence of specific ERV insertion sites; those sites form a nested hierarchy when you compare species. To buttress this, the degree to which ERV insertion sites are shared across species matches extremely well how old the ERV insertions are, based on the number of mutations in their terminal repeats.

Are you ever going to deal with the real argument, rather than all of this other stuff?

I hadn't seen a lot of compelling evidence that proved or disproved common ancestry one way or the other. ERVs have their favorite insertions points, 'hotspots' just like mutations do. Ran into this one with the pseudogene arguments, there are places that are more susceptible to mutations. I did field the evidence he was presenting but it seemed rather limited and anecdotal. I've seen this rather uninteresting line of evidence

Phylogenies of seven HERV loci

Ok, that's seven, maybe as many as ten. My reaction to the whole thing was so what?

I'm only dealing with the argument you're presenting here. Whether someone else has presented a different wrong argument somewhere else has nothing to do with it.

I really just wanted it established that we are talking about 8% of the respective genomes. I also wanted to make it clear that the Pterv represents a million base pairs, again, no big deal but I wanted that made clear. I have ran into this time and time again. It's like the indels and the overall divergence, the 3-4% divergence based on them is a very big deal. The problem is I get corrected on things that are really just semantics so I end up chasing down these kind of trivialities.

My actual ideas about ERVs is that I find it very difficult to fathom how 8% of the genome is actually just accumulated viruses. I never really bought into that. I don't mind looking closer at these arguments even though they seem a little pedantic.

The only evidence you've presented here suggests that the only difference between 4% (5%, actually, since the number was 4.6%) and 8% is what exactly is being counted as an ERV. Mind you, if estimates of the fraction really did range between 4% and 8% it wouldn't be particularly interesting, but all of these numbers seem to be based on a single study.

I thought you just told me it was 8%. Ok, the MaLRs aren't really ERVs, just kind of related no big deal. It's like asking you if we are the 98% the same in our DNA as the Chimpanzee, you just say it all depends. What I have come to realize it's that it only depends on whether or not you want to count the indels.

No, I really, really don't see a problem. That's why I said I didn't see a problem. That's why I asked you what the problem is. Are you going to reveal the problem soon? So far everything you've said seems to be perfectly consistent with standard evolutionary accounts.

I just wanted to know the length of the ERVs and the percentage of the genomes they represent. It sounds like you saying there are ~29 Mbps worth of class 1 ERV in the human genome and the Ptervs come to about 1 Mbps. It's not a problem, I just don't think it should be an open question.

You introduced this subject by saying you were refuting the argument for common descent from ERVs. You haven't refuted anything here. The only thing you've pointed out is that some LTRs can be classified in different ways and so show up in different lines of summary charts.

Not sure how I worded it but the ERVs are far and away the worst homology argument I have ever seen. I don't know if that's a refutation because I'm not sure it's an argument.

Steve, I have always appreciated you input into these discussions. The truth is that I couldn't be more grateful. My only real interest in genetics is the basis for adaptive evolution, I think the ERVs are proof of very little to be totally honest. As a matter of fact, I don't think comparative genomics offers us any real substantial proof one way or the other. That's just how I feel about it. LM and I had danced with this one for weeks when I finally badgered him into a formal debate, I thought it would put this whole ERV thing behind us. He asked be to take up the topic more then once, I don't know exactly why it's important to him but he asked nicely so here I am.

Oh and BTW, how you liking Harvard? Do you miss MIT?

Grace and peace,
Mark

 

[mark kennedy]

(Don't mind me butting in again )



Tomk80 has already mentioned Dr. Dart's reasoning on why they think the Taung child is a human ancestor rather than just an ape (as well as other anatomical differences such as the size of the incisors), but I'd like to add more.

The Taung Child - an infant specimen of Australopithecus Africanus - still has a partly-open metopic suture: a thin band of cartilage that separates the two frontal bones in the skull, and is responsible (along with other sutures) for giving the child a fontanelle or "soft spot". In infant chimps is closes shortly after their first teeth emerge, whereas in humans (because the brain continues to grow greatly after birth) it remains munch longer.

The Taung Child was estimated to have been around 3 or 4 years old when it died. If it was a chimpanzee the metopic suture would have been fused by this time. The fact that it still had a partly-open suture long after birth suggested a more human-like pattern of brain growth.

The type specimen for Australopithecus africanus (Taung) includes a natural endocast that reproduces most of the external morphology of the right cerebral hemisphere and a fragment of fossilized face that articulates with the endocast. Despite the fact that Taung died between 3 and 4 y of age, the endocast reproduces a small triangular-shaped remnant of the anterior fontanelle, from which a clear metopic suture (MS) courses rostrally along the midline ... In great apes, the MS normally fuses shortly after birth, such that unfused MS similar to Taung’s are rare. In humans, however, MS fuses well after birth, and partially or unfused MS are frequent. In gracile fossil adult hominins that lived between 3.0 and 1.5 million years ago, MS are also relatively frequent, indicating that the modern human-like pattern of late MS fusion may have become adaptive during early hominin evolution.​

Metopic suture of Taung - pnas.org​

​

Darn it!!! It's just getting interesting and I'm getting bogged down with other things. That's why I had to give these debates up, I can't do this all the time and have a life.

Just bear with me, I'll get to this one for sure, I just don't have the time right now.

 

[46AND2]

LM and I had our debate back in 2007. Then, like now, he had real problems getting current facts and figures. Not much has changed so the arguments are going to be about the same.



They are one of the most abundant families of ERVs and they are absent in the Human Genome. They account for 7% of the divergence due to indels, which accounts for 3-4% of the divergence overall. This isn't much of an argument, as a matter of fact, I think it's a pretty strong argument against common ancestry.



There are 200,000 copies in the human genome according to the Human Genome paper. The table I think LM got his statistics concerning ERVs in the Human Genome reports just over 100 families and just over 200 subfamilies. You are mixing up families with copies.

How am I suppose to take these arguments seriously when I'm constantly dealing with bogus statistics?



Going to need to know where your getting your information.



If it makes perfect sense then why was it surprising to the Chimp Genome researchers, 'to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2)'?

It also says the 'the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human'.

Perfect sense? I really don't follow the logic at all.

No sir, you are getting confused. From the paper which you said claimed 100 families of PtERV ERVs:

We report here that the chimpanzee genome contains at least 42 separate families of endogenous retroviruses, nine of which were not previously identified. All but two (CERV 1/PTERV1 and CERV 2) of the 42 families of chimpanzee endogenous retroviruses were found to have orthologs in humans.

Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses

First of all, it says 42 families (and not all of them are PtERV1), and only 2 are not orthologous (PtERV1 is one, CERV2 is the other).

The PTERV1 family has 100 members, not 100 families.

PtERV1 is one family with 100 members. It is one of those 2 non-orthologous families.

Only 2 families out of the 42 from this paper are chimp-specific, and 100 individual PtERV1 members out of the 425 that they looked at. And the reason this makes sense is that of the 425 which are fixed recently enough to have remained full-length, a large portion of those occurred since the divergence of humans and chimps.

But when you take all ERVs into account, including the fragmented ones, a much higher percentage of them are shared between the two species. This is indicative of the fact that older ERVs, the ones which fixed prior to the split of the lineages, are much more likely to be fragmented.



Also: I would like to add that the paper you cited, and I re-cited in this post, does NOT state that the PtERV family is THE most abundant in the genome, as you stated. It specifically says ONE OF the most abundant.

 

[USincognito]

Mark, we can get back to our Taung tangent later, but for now I wanted to try a layman to layman approach on ERVs (and I know I've done this before).


- The number of bases, the percentages, the numbers in families, mutations, etc. etc., are diversions from what makes ERVs evidence for common ancestry.
- There is a difference between orthologous (in the same place) and non-orthologous (in different places) ERV insertions.

Orthologous - GGGV1GGV2GGGGV3G
Non-orthologous - GGGV2GGGGGV4GV3G

- The orthologous ones are important because they form a nested hierarchy when humans are compared to other primates.

Ex.
Every Haplorhine has ERV1, but not all of them have ERV2-6.
Every Catarrhine has ERV1 and 2, but not all of them have ERV3-6.
Every Orangutan has ERV1, 2 and 3, but lack ERV4-6.
Every Gorilla has ERV1-4, but lacks ERV5 and 6.
Every Chimpanzee has ERV1-5, but lacks 6.
Every Human has ERV1-5 as well as 6.

Such a pattern - when the ERVs are inserted into orthologous positions - forms a nested hierarchy that is indicative of common ancestry and really doesn't have a scientific explanation other than common ancestry.

 

[Loudmouth]

Don't understand? My whole argument is based on the divergence which is by definition 'lineage specific' in the respective genomes.

So if there are 200,000 human ERV's and only 100 are lineage specific, how many are shared with chimps?

The fact is that you can't be trusted to get the facts straight, you never have been.

I have had the facts straight from the very start of this thread.

For us to share a lot of DNA with Chimpanzees really prove very little, makes a nice homology argument but that's about it. What you need is a molecular basis for adaptive evolution. You seem to forget, we have a brain three times bigger then a chimp.

Then we are no longer talking about the topic of this thread. Do you conceed that of the 200,000 ERV's in our genome we can find all but 100 of them at orthologous positions in the chimp genome?

Also, you have yet to show us an evidenced mechanism that can produce orthologous insertions through independent infections in 99.9% of insertions. You have yet to explain why orthology falls into the nested hierarchy predicted by evolution. You have yet to explain why LTR divergence is consistent with evolution predictions.

It matters little to me which ones we look at. My interest is where they are, the size of the sequences, what they actually do and whether or not this has anything to do with common ancestry.

Your interest has been to obfuscate and ignore their position in the genome.

 

[Loudmouth]

ERVs have their favorite insertions points, 'hotspots' just like mutations do. Ran into this one with the pseudogene arguments, there are places that are more susceptible to mutations. I did field the evidence he was presenting but it seemed rather limited and anecdotal. I've seen this rather uninteresting line of evidence

Phylogenies of seven HERV loci

Ok, that's seven, maybe as many as ten. My reaction to the whole thing was so what?

Are you saying that if common ancestry is true that ERV's should not be found at orthologous positions, they should not fall into a nested hierarchy, and that LTR divergence should not mirror the phylogeny?

Please give us specific reasons why this is is not evidence.

First, the distribution of provirus-containing loci among taxa dates the insertion. Given the size of vertebrate genomes (>1 × 10^9 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).
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We have 200,000 such markers.

I really just wanted it established that we are talking about 8% of the respective genomes.

We are talking about hundreds of thousands of independent genetic markers that can be used to determine if humans and chimps share a common ancestor.

It's like the indels and the overall divergence, the 3-4% divergence based on them is a very big deal.

Why is it a big deal?

My actual ideas about ERVs is that I find it very difficult to fathom how 8% of the genome is actually just accumulated viruses. I never really bought into that.

And you complain about me getting my facts wrong?

Ok, the MaLRs aren't really ERVs, just kind of related no big deal. It's like asking you if we are the 98% the same in our DNA as the Chimpanzee, you just say it all depends. What I have come to realize it's that it only depends on whether or not you want to count the indels.

If you count indels, chimps are still our closest relative. Even more interesting, we are the chimps closest relative. Chimps are more distantly related to other apes than they are to us.

Not sure how I worded it but the ERVs are far and away the worst homology argument I have ever seen.

Why?

My only real interest in genetics is the basis for adaptive evolution, I think the ERVs are proof of very little to be totally honest.

Why are ERV's not proof of common ancestry?

As a matter of fact, I don't think comparative genomics offers us any real substantial proof one way or the other. That's just how I feel about it. LM and I had danced with this one for weeks when I finally badgered him into a formal debate, I thought it would put this whole ERV thing behind us. He asked be to take up the topic more then once, I don't know exactly why it's important to him but he asked nicely so here I am.

Why is it important to you to use smoke and mirrors to discount the number of ERV's shared by humans and chimps?

 

[Notedstrangeperson]

If you count indels, chimps are still our closest relative. Even more interesting, we are the chimps closest relative. Chimps are more distantly related to other apes than they are to us.

With one exception - chimps and bonobos are more closely related to one another (sharing 99.6% of their DNA) than chimps are to humans (link). After all, bonobos are estimated to have split from chimps around 2.5 million years ago, long after humans and chimps started going their separate ways around 5-7 million years ago.

Interestingly, bonobos share about the same amount of DNA with humans as chimps do (around 98.7% according to the link above). I wonder why? You'd think we would share less DNA with them than we do with chimpanzees, considering we diverged from chimps earlier than they did.