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Another poor response to ERV evidence for common ancestry by a creationist.

Zaius137

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Blayz...

I suppose the citations were not clear enough to say that these examined sequences were created at the time of insertion and particular to the provirus. Knowing the quality of the participants here I did not see the need. When you can not adequately answer the core questions it is sometimes beneficial to misquote the opponent. I forgive you.
 
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Blayz

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Blayz...

I suppose the citations were not clear enough to say that these examined sequences were created at the time of insertion and particular to the provirus.


Yes, that is one of the major points supporting them as evidence of evolution. Well done on finally conceding this point.


Knowing the quality of the participants here I did not see the need. When you can not adequately answer the core questions it is sometimes beneficial to misquote the opponent. I forgive you.

I didn't misquote you. You said

Excuse me but the LTR’s are generated upon insertion…. Get that fact threw your head. They belong to the provirus only by the action of reverse transcription. They are not in the central viral genome. You missed that point altogether.

The bolded part is utter rubbish. They are indeed in the viral genome, they just happen to not be in the same location.
 
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Zaius137

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Blayz..

Excuse me but the LTR’s are generated upon insertion…. Get that fact threw your head. They belong to the provirus only by the action of reverse transcription. They are not in the central viral genome. You missed that point altogether.


“The bolded part is utter rubbish. They are indeed in the viral genome, they just happen to not be in the same location.”

Or the same configuration, they are in quite a different form in the retrovirus. The LTRs are literally built from patterns on the retrovirus in response to “vanishing promoters”. Nothing I stated is inconsistent with the facts. The LTRs (not the core provirus) are the regions examined for mutational changes supporting common ancestry.

The core provirus mutation rate also disagrees with the LTR rate of mutation.

“In both cases, LTR sequences evolved in sequence independently from, and obviously more rapidly than, the proviral bodies. Reasons for apparently different evolutionary rates of LTRs and proviral bodies are currently not clear.”

This fact only amplifies my objection. The question you need to answer is why are the regions even recognizable at all given the astounding rate of observed mutations of retroviruses today? As I cited earlier:

“ In addition, the HIV reverse transcriptase enzyme makes many mistakes while making DNA copies from HIV RNA. As a consequence, many variants of HIV develop in an individual, some of which may escape destruction by antibodies or killer T cells. Additionally, different strains of HIV can recombine to produce a wide range of variants or strains.”

http://www.bloodindex.org/mutation_hiv.php

This type of thing is common with retroviruses.

Again…

In the case of HERV-k it is claimed that the infection happened just after the chimp human divergence and continued up until 100,000 years ago. That is on the order of about 5 million years according to the tale. You literally have an ape like hominid turn into a human but the HERV-k stays literally intact, enough so as to be put back together???

The GaG, PoL, and EnG still look like the HERV-K. So your telling me that a ape like hominid changed into a modern human but the HERV-K virus (with an astounding mutation rate) stayed a HERV-K virus. Then that virus mysteriously went extinct 100,000 years ago even thou the human population increased; more hosts more viral infections.

If you can still say that ERV’s support evolution I can still say you are nuts.
 
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mark kennedy

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I have always wondered if them being the same in the respective genomes is such a good homology argument, what if they were very different? That would be an argument for independent lineages?

Blayz..

In the case of HERV-k it is claimed that the infection happened just after the chimp human divergence and continued up until 100,000 years ago. That is on the order of about 5 million years according to the tale. You literally have an ape like hominid turn into a human but the HERV-k stays literally intact, enough so as to be put back together???

The GaG, PoL, and EnG still look like the HERV-K. So your telling me that a ape like hominid changed into a modern human but the HERV-K virus (with an astounding mutation rate) stayed a HERV-K virus. Then that virus mysteriously went extinct 100,000 years ago even thou the human population increased; more hosts more viral infections.

If you can still say that ERV’s support evolution I can still say you are nuts.

That's the first time I have seen a homology argument turned on itself. Anyway, once the retrovirus gets introduced to the genome I would expect it would be preserved like any other sequence. What is mysterious about the ERV germline invasion, at least for me, is how they get into the germline at all. I have to be more then a little incredulous about 8% of the human genome being the result of viral invasions.

It's still fascinating that no matter how bad the homology argument is, it still must be the case because the alternative is unthinkable.

Grace and peace,
Mark
 
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Blayz

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Or the same configuration, they are in quite a different form in the retrovirus. The LTRs are literally built from patterns on the retrovirus in response to “vanishing promoters”. Nothing I stated is inconsistent with the facts. The LTRs (not the core provirus) are the regions examined for mutational changes supporting common ancestry.

They are absolutely in disagreement with the facts. LTRs are entirely derived from virus sequence, and both termini are the same upon insertion. We can therefore use the independent evolution of the LTRs as a measure. Examining these regions for mutational changes to support common ancestry is entirely valid.

The core provirus mutation rate also disagrees with the LTR rate of mutation.
“In both cases, LTR sequences evolved in sequence independently from, and obviously more rapidly than, the proviral bodies. Reasons for apparently different evolutionary rates of LTRs and proviral bodies are currently not clear
This is the only valid observation you have made so far.

The question you need to answer is why are the regions even recognizable at all given the astounding rate of observed mutations of retroviruses today? As I cited earlier:
Because there is a limit to the amount of mutation that can be borne before the element loses functionality, the same reason we can identify similar genes between humans and bacteria. You don't need to tell me the virus mutates rapidly. Unlike you I have actually sequenced HIV samples. You know, done actual work rather than whinging about other people's on a public forum.

In the case of HERV-k it is claimed that the infection happened just after the chimp human divergence and continued up until 100,000 years ago. That is on the order of about 5 million years according to the tale. You literally have an ape like hominid turn into a human but the HERV-k stays literally intact, enough so as to be put back together???
What's the problem? The difference between chimp and human is ~5%. Since the virus is sitting in the genome, why wouldn't it be intact if it has only diverged 5% ?

The GaG, PoL, and EnG still look like the HERV-K. So your telling me that a ape like hominid changed into a modern human
As the result of a 5% change, give or take

but the HERV-K virus (with an astounding mutation rate) stayed a HERV-K virus.
What do you want it to turn into, an elephant? The virus mutates around a mean. I daresay you are forgetting the selection part of the equation again.

Then that virus mysteriously went extinct 100,000 years ago even thou the human population increased; more hosts more viral infections.
I don't have the data on the human population 100 000 years ago. perhaps you'd like to provide some evidence it was increasing at that time. Before that, which bit of the paper are you getting this 100 000 years ago bit from? the introduction states the activity stopped just after the split.

If you can still say that ERV’s support evolution I can still say you are nuts.
ERVs support evolution. Your incredibly low incredulity threshold is not a yardstick by which we measure reality.

"I don't understand it, Goddidit" is all you are saying, and as is typical of your ilk rather than getting out there and doing work you just want to whinge about other people's.

Was a better quality post than your memory guards one though. I note you blithely ignored responses to that.
 
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Blayz

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I have always wondered if them being the same in the respective genomes is such a good homology argument, what if they were very different? That would be an argument for independent lineages?

Yes

I have to be more then a little incredulous about 8% of the human genome being the result of viral invasions.

You should stop there then. Everyone knows, once you have hit your incredulity threshold, the correct response is Goddidit. Absolutely no other thought or investigation is required.

It's still fascinating that no matter how bad the homology argument is, it still must be the case because the alternative is unthinkable.

Naah, it's your crowd that does the unthinkable thing. We'd be happy to think it if there was evidence for it.

Homology could also put forward common design.

Mark understands the meaning of the word homology. You do not. Homology in the biological sense means quite literally "related by descent". Related by descent is the opposite argument to common design.
 
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Loudmouth

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Excuse me but the LTR’s are generated upon insertion…. Get that fact threw your head. They belong to the provirus only by the action of reverse transcription. They are not in the central viral genome. You missed that point altogether.

They are still part of the viral genome, and they are copied from the RNA genome to the DNA genome and then back to the RNA viral particle. During this process, the 5' LTR (if memory serves) is used to produce the 3' LTR so that they are identical at the time of insertion.

“Owing to the retroviral reverse transcription strategy, both LTR sequences are identical in sequence at the time of provirus formation.”
That’s from your article… Remember the LTRs are removed to produce the phony resurrected virus… snip, snip.


So what is the reverse trascriptase transcribing from? Do tell. Where do the LTR's come from according to you?

Ten families were identified? If you believe they can not evolve outside 10 families in 30 million years (remember they are retroviruses) I guess you can also believe in evolution. By the way where do you Darwinists meet for fellowship?

Moving the goalposts I see. You claimed that they didn't evolve. They did.

Evolution is religion not observable science. You still pay homage to mischievous leprechauns and magic (central to your origin fairytales).

Who is the one proposing that life was produced by a supernatural deity who spoke it into existence (i.e. incantation)? It's not me. I am pointing to observed and testable natural mechanisms, not magic.

Remember I showed where the HERV-k con (as in conman) does not insert like MMTV and does not have the functionality of the MMTV. So forget about claiming that it is a viable reconstructed virus in that genus.

Why would HERV-Kcon need to insert like MMTV? It inserts like HERV-K as shown by identical insertional patterns for HERV-Kcon and observed HERV-K in the human genome.

Your citation still does not show how a retrovirus can survive virtually unchanged 5-30 million years and still be identified as HERV-K; the suggestion of that happening is absurd.

It didn't survive virtually unchanged. That is your fairtytale.

“In both cases, LTR sequences evolved in sequence independently from, and obviously more rapidly than, the proviral bodies. Reasons for apparently different evolutionary rates of LTRs and proviral bodies are currently not clear.”
It will not be clear until they drop that fossil virus nonsense.

You have yet to show that it is nonsense.
 
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Loudmouth

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I have always wondered if them being the same in the respective genomes is such a good homology argument, what if they were very different? That would be an argument for independent lineages?

Yes, it would. If these retroviruses inserted independently into chimp and human genome then we would not expect 99% of them to be found at orthologous positions, nor would we expect a larger comparison between primates to produce an ERV phylogeny that matches the morphological phylogeny.

The same applies for the common design argument. The common design argument does not predict a nested hierarchy for orthology, LTR divergence, and overall sequence divergence. The common design argument actually makes no predictions and is both untestable and unfalsifiable. All we keep hearing is that God made it look like evolution occurred for no discernable reason. God would not be limited to a nested hierarchy. God would not be forced to produce ERV's so that an ERV shared by all apes would have higher LTR divergence than an ERV found only in humans. God would not be forced to include an ERV in chimps if it is also found in humans and orangutans. The nested hierarchy is inexplicable in the common design argument. However, the nested hierarchy is exactly what we should see if evolution is true.

What is mysterious about the ERV germline invasion, at least for me, is how they get into the germline at all. I have to be more then a little incredulous about 8% of the human genome being the result of viral invasions.

At least you admit that your argument is based on a fallacy, an argument from incredulity.

It's still fascinating that no matter how bad the homology argument is, it still must be the case because the alternative is unthinkable.

The alternative is untestable and unfalsifiable. It is the same as claiming that fingerprint evidence should be dismissed because Leprechauns could have produced them at the scene of the crime.
 
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Loudmouth

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Homology could also put forward common design.

Just like leprechauns planting evidence at the scene of a crime could be put forward during a trial. I wouldn't recommend it, but it could be put forward.

The facts remain that we have a known and observable mechanism that produces endogenized retroviruses. Guess what that mechanism is? You got it. RETROVIRUSES. So why would we throw that mechanism out in favor of an unobserved, unevidenced, and untestable mechanism that is supported solely by religious belief? Oh, and this mechanism also has the added feature of producing ERV patterns that are identical to retroviral insertion and evolution to top it all off.
 
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mark kennedy

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Homology could also put forward common design.

I have always thought that the Big Bang makes a pretty good argument for creation, if you don't assume naturalistic causes from the beginning. Anyway, I know what your saying about homology arguments, perhaps some things should be different is we are looking at gradual successive changes. I like the approach, I'll be watching the thread.

Grace and peace,
Mark
 
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mark kennedy

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Yes, it would. If these retroviruses inserted independently into chimp and human genome then we would not expect 99% of them to be found at orthologous positions, nor would we expect a larger comparison between primates to produce an ERV phylogeny that matches the morphological phylogeny.

Nonsense, there is not that much commonality and of the 3% that represents the major genetic differences between chimpanzees and humans, 7% is due to indels in these ERVs. Once they are in the genome they will, or should, be conserved like any other sequence. What you would not expect is for the largest most abundant families of ERVs to be present in species that are not as closely related. The largest family of ERVs in the chimpanzee genome must have been acquired independently and that's not my opinion, there is no other explanation.

PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species. (Initial Sequence of the Chimpanzee Genome, Nature 2005)​

Separate germline invasions, so we know it's not only possible, we know it happened here.

The same applies for the common design argument. The common design argument does not predict a nested hierarchy for orthology, LTR divergence, and overall sequence divergence. The common design argument actually makes no predictions and is both untestable and unfalsifiable. All we keep hearing is that God made it look like evolution occurred for no discernable reason. God would not be limited to a nested hierarchy. God would not be forced to produce ERV's so that an ERV shared by all apes would have higher LTR divergence than an ERV found only in humans. God would not be forced to include an ERV in chimps if it is also found in humans and orangutans. The nested hierarchy is inexplicable in the common design argument. However, the nested hierarchy is exactly what we should see if evolution is true.

Everything you are saying is untestable and unfalsifiable. You nurse this theory that they are so much alike that common ancestry is the only explanation. Then when you find out that the ERVs make up 8% of the respective genomes instead of the 1% you originally thought your argument does not miss a beat. Nothing you are arguing has in inverse logic, or don't even make adjustments.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006).​

CERV 1/PTERV1 and CERV 2 do not have orthologs, the others have them but the sequences are far from identical as I have heard you argue foolishly and recklessly. What you don't seem to appreciate is that your homology argument is that you have to be ready to concede the divergence that undermines your anticipated commonality. This kind of a study does not predict ERVS, their character and function, based on common ancestry. That is a shallow, fallacious and completely indefensible position but you evolutionist buddies will let you argue it for one reason. They have no other option, they have to organize the evidence around their naturalistic assumptions.



At least you admit that your argument is based on a fallacy, an argument from incredulity.

I'm not incredulous in the slightest, the evidence is indicating a vast level of divergence you won't honestly admit and can't possibly account for. The biggest fallacy in this whole thing is the circular reasoning that uses the same tired old Darwinian rhetoric, loosely garnished around a deep, abiding hostility for religion and theistic reasoning. It has nothing to do with the great epistomological revolution and inversion that has guided natural science for centuries.

You are not arguing from science, you are and have always argued from presumption claiming fullfilled predictions that were never made and homology arguments that never deliver real world molecular mechanisms involved in major morphological innovations.

The alternative is untestable and unfalsifiable. It is the same as claiming that fingerprint evidence should be dismissed because Leprechauns could have produced them at the scene of the crime.

Common ancestry is untestable and unfalsifiable what's your point, this is philosophy not empirical testing and I find your lack of candor along these line to be something close to a closed mouth admission.
 
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mark kennedy

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ERVs support evolution. Your incredibly low incredulity threshold is not a yardstick by which we measure reality.

"I don't understand it, Goddidit" is all you are saying, and as is typical of your ilk rather than getting out there and doing work you just want to whinge about other people's.

Was a better quality post than your memory guards one though. I note you blithely ignored responses to that.

I'm not getting that from the scientific literature and research. What I get are these elaborate homology arguments that fall apart because evolutionists will not accept the known alternative to exclusively naturalistic causes. Perhaps I am nursing some ignorance of scientific methods but I never dispute evidence that has been reasonably and properly determined. What is more I have always accepted the inverse logic for my views and sought out alternatives, I just retain the right to remain unconvinced as we all should if the evidence is still dubious.

Where we are in conflict is what the significance of the ERVs, as they exist in the respective genomes, indicate common ancestry. The largest most abundant families of ERVs in the chimpanzee genome has not orthologs in the human genome. Sooner or later you are going to have to honestly admit that there is no way that this was predictable given an assumption of common ancestry. The rest is speculation added post hoc, this isn't due to science, this resulted from bias.

Gee I'm glad I finally got these crazy debates out of my system.
 
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Loudmouth

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Nonsense, there is not that much commonality and of the 3% that represents the major genetic differences between chimpanzees and humans, 7% is due to indels in these ERVs. Once they are in the genome they will, or should, be conserved like any other sequence.

Actually, no they shouldn't. First, you have repetitive sequence at either end of the ERV's which are the LTR's. Repetitive sequences lend themselves to recombination events. Therefore, there will be more recombination events at LTR's compared to non-repetitive DNA elsewhere in the gneome.

Second, retroviral insertions may very well be deleterious. This would lead to selection of mutations such as indels.

What you would not expect is for the largest most abundant families of ERVs to be present in species that are not as closely related.

There are only a few hundred PtERV insertions in chims and gorillas, none of which are orthologous. This compares to the over 200,000 ERV's in chimps.

The largest family of ERVs in the chimpanzee genome must have been acquired independently and that's not my opinion, there is no other explanation.
PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species. (Initial Sequence of the Chimpanzee Genome, Nature 2005)
Separate germline invasions, so we know it's not only possible, we know it happened here.

Yes, and all of these insertions are non-orthologous just as the theory of evolution predicts. This prediction was made by looking at the distribution of PtERV insertions amongst primates. If evolution is true then PtERV insertions should be found at non-orthologous positions, and they are.

Everything you are saying is untestable and unfalsifiable.

So we can't test to see if insertions are found at an orthologous base in each genome? Every geneticist I know will completely disagree. The predictions are testable, and they have been tested. They passed.

You nurse this theory that they are so much alike that common ancestry is the only explanation.

Another empty accusation.

Then when you find out that the ERVs make up 8% of the respective genomes instead of the 1% you originally thought your argument does not miss a beat.

The argument is not based on percentages. It is based on orthology and divergence. You might as well claim that finding 8 fingerprints instead of 1 fingerprint at a crime scene somehow negates the evidence. It doesn't.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006).

There are over 200,000 ERV's in the chimp genome. PtERV insertions make up less than 1% of all ERV's.

CERV 1/PTERV1 and CERV 2 do not have orthologs,

Which they shouldn't if evolution is true. That you don't understand that only highlights your ignorance of how evolution works.

What you don't seem to appreciate is that your homology argument is that you have to be ready to concede the divergence that undermines your anticipated commonality.

Zaius claims just the opposite. You guys need to get together and form a consistent argument.

This kind of a study does not predict ERVS, their character and function, based on common ancestry. That is a shallow, fallacious and completely indefensible position but you evolutionist buddies will let you argue it for one reason. They have no other option, they have to organize the evidence around their naturalistic assumptions.

So you are saying that all of these scientists are fudging the data to make the ERV's appear to be orthologous? What exactly are you arguing against? You seem to be tilting at windmills.

I'm not incredulous in the slightest,

"I have to be more then a little incredulous about 8% of the human genome being the result of viral invasions."--mark kennedy

Will the real mark kennedy please step forward?

the evidence is indicating a vast level of divergence you won't honestly admit and can't possibly account for.

It seems you can't cite it either.

The biggest fallacy in this whole thing is the circular reasoning that uses the same tired old Darwinian rhetoric, loosely garnished around a deep, abiding hostility for religion and theistic reasoning. It has nothing to do with the great epistomological revolution and inversion that has guided natural science for centuries.

More empty assertions.

You are not arguing from science, you are and have always argued from presumption claiming fullfilled predictions that were never made and homology arguments that never deliver real world molecular mechanisms involved in major morphological innovations.

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).
http://www.pnas.org/content/96/18/10254.full
There is the prediction. You can stop claiming it doesn't exist now.

Common ancestry is untestable and unfalsifiable

The test is described in the ERV paper above.
 
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Loudmouth

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What I get are these elaborate homology arguments that fall apart because evolutionists will not accept the known alternative to exclusively naturalistic causes.

What known alternatives? When has anyone every observed a supernatural deity inserting retroviral genes into the genome of an entire species? Can you name a single instance? If not, then there is no alternative.

You are once again citing the equivalent of leprechauns planting fingerprints at a crime scene.

Perhaps I am nursing some ignorance of scientific methods but I never dispute evidence that has been reasonably and properly determined.

You are ignoring observed mechanisms for insertion of retroviral DNA into host genomes for a mechanism that has never been observed. How is this reasonable or proper?

Also, if evolution is true are you saying that there should be no homology between chimps and humans? Are you saying that evolution does not produce a nested hierarchy? Are you saying that the DNA similarities between you and your siblings is due to a supernatural deity poofing you both into existence, or is it due to a common ancestor?

I just retain the right to remain unconvinced as we all should if the evidence is still dubious.

You have the right to your own opinion, but you do not have the right to your own facts. That is the problem. You act as if magical poofing is a scientific alternative. It isn't. It never was. At the same time, you simply ignore the natural mechanisms that produce retroviral insertions, and even then you distort the facts.

Where we are in conflict is what the significance of the ERVs, as they exist in the respective genomes, indicate common ancestry.

If common ancestry is true, are you saying that no ERV's should be found at orthologous positions?

The largest most abundant families of ERVs in the chimpanzee genome has not orthologs in the human genome.

PtERV's make up less than 1% of all ERV insertions in the chimp genome. On top of that, there are no PtERV insertions in humans, much less orthologous ones. There are insertions in other primates. From this data alone I can use the theory of evolution to predict that PtERV insertions should not be found at orthologous positions in apes. The distribution between species indicates independent insertion after common ancestry, and this is once again confirmed by experimental testing. Why is that?

If these PtERV inserted into the common ancestor of chimps and gorillas then humans should have them too. They don't. Humans do not have any PtERV insertions. Therefore, the insertions did not occur in that common ancestor. They happened after those lineages branched off from one another. This means that the theory of evolution would predict that PtERV insertions between chimps and gorillas (and other primates) should NOT be orthologous since they occurred independently. THAT IS THE TEST. What does the test show? They are non-orthologous just as the theory predicted.

That you don't understand this is your own problem. If you don't understand how cladistics and a nested hierarchy works and the predictions you can make with these tools then you need to study up.

Sooner or later you are going to have to honestly admit that there is no way that this was predictable given an assumption of common ancestry.

Why would I admit something that isn't true? Why would I want to join you in your ignorance of how science works?
 
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Loudmouth

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mark kennedy,

Just so this doesn't get buried I would like to walk through the PtERV predictions step by step. I will ask some very simple questions, and I will show you how the answers lead to the predictions in a very obvious way.

First question. According to the theory of evolution do chimps, humans, and gorillas share a single common ancestor? That is, according to the theory does the chimp/human clade branch off from gorillas? Keep in mind, I am not asking you to agree that common ancestry is true, only agree that this is what the theory states.
 
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mark kennedy

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Actually, no they shouldn't. First, you have repetitive sequence at either end of the ERV's which are the LTR's. Repetitive sequences lend themselves to recombination events. Therefore, there will be more recombination events at LTR's compared to non-repetitive DNA elsewhere in the genome.

I get the logic just not the relevance. This point of clarification is something I found helpful:

multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (cited and linked below)​

The question then becomes how common is it. First you would determine the amount of ERVs in a genome, so what is it for you now, 1%, 4% or 8%. I only ask because when our debate ended you were stuck at 4% and some change.

Second, retroviral insertions may very well be deleterious. This would lead to selection of mutations such as indels.

Selection of mutations whether insertions, deletions, point or rearrangements are most often deleterious when they have an effect strong enough for selection to act. What their connection is to molecular mechanisms that effectively alter the traits of a species is speculative. One thing is clear, to me at least. The DNA repair mechanisms are far more common in genomes then ERVs.

There are only a few hundred PtERV insertions in chims and gorillas, none of which are orthologous. This compares to the over 200,000 ERV's in chimps.

Just the largest and most abundant families of ERVs in the Chimpanzee genome, no big deal right? I have seen some bad homology arguments before but this one gets worse as it goes.

Yes, and all of these insertions are non-orthologous just as the theory of evolution predicts. This prediction was made by looking at the distribution of PtERV insertions amongst primates. If evolution is true then PtERV insertions should be found at non-orthologous positions, and they are.

You left out the null hypothesis, that's just another form of begging the question. Anyway, you are throwing words around without ever bothering to say what they actually mean. It would not be so bad it you did not do it so often.

The term orthologous segment is defined as a set of genomic segments in different organisms descended from a common ancestor without large rearrangements (Dewey et al., 2006).​

That is classic circular reasoning, it is from a common ancestor so if we find it in the sequence it proves common ancestry. The fact of the matter is that they are called orthologous because they are so much alike, it's as simple as that. You would not find them at orthologous locations because if they were significantly different they wouldn't be called orthologous. Your being fallacious.

So we can't test to see if insertions are found at an orthologous base in each genome? Every geneticist I know will completely disagree. The predictions are testable, and they have been tested. They passed.

They were compared dude, just like indels in comparative genomics don't have to be the result of insertions or deletions. Not if the genomes are independently created. They are simply differences and if you want to compare the things that are the same and offer them as proof you have to account for the differences.

The argument is not based on percentages. It is based on orthology and divergence. You might as well claim that finding 8 fingerprints instead of 1 fingerprint at a crime scene somehow negates the evidence. It doesn't.

We are not talking about fingerprints, we are talking about sequences that are prone to mutations. You are talking about fragments in a lot of cases and pretending they are all broken in the same place, that's really shallow. What is worse is that you are so short on particulars.

There are over 200,000 ERV's in the chimp genome. PtERV insertions make up less than 1% of all ERV's.

This one is refreshingly honest:

Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists. Yohn et al, 2005



Which they shouldn't if evolution is true. That you don't understand that only highlights your ignorance of how evolution works.


I understand that you are very clumsy with the facts and vague with your terminology. I understand something about evolution you don't, the fact of the matter it is used in at least two different ways at the same time, a fallacy known as equivocation.

Zaius claims just the opposite. You guys need to get together and form a consistent argument.

Zaius raises and interesting point, other then that was are discussion very different things.

So you are saying that all of these scientists are fudging the data to make the ERV's appear to be orthologous? What exactly are you arguing against? You seem to be tilting at windmills.

Not appear, but are orthologous, meaning the sequences are the same.

"I have to be more then a little incredulous about 8% of the human genome being the result of viral invasions."--mark kennedy

Will the real mark kennedy please step forward?

Do you agree that it's 8% at least?.

That will do for now, thanks for the fish in the bowl target practice.

Have a nice day :)
Mark
 
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Loudmouth

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The question then becomes how common is it. First you would determine the amount of ERVs in a genome, so what is it for you now, 1%, 4% or 8%. I only ask because when our debate ended you were stuck at 4% and some change.

Let's use the value from the best set of data which is the human genome paper. They reported ~200,000 ERV's comprising 8% of the human genome, specifically in table 11 found here:

Table 11 : Initial sequencing and analysis of the human genome : Nature

We can then look at the chimp genome paper which compared the ERV's from the chimp and human genomes. That table can be found here:

Table 2 : Initial sequence of the chimpanzee genome and comparison with the human genome : Nature

So of the ~200,000 ERV's in the human genome only 82 of them could not be found at an orthologous position in chimps. Of the ERV's found in chimps, only 279 could not be found at an orthologous position in humans (this includes PtERV insertions). More than 99% of ERV's in each genome are at orthologous positions. Those are the facts. The facts are in the essay linked in the opening post. They are the facts discussed throughout the beginning of the thread when you were participating.

Just the largest and most abundant families of ERVs in the Chimpanzee genome, no big deal right?

There are around 200 PtERV insertions in the chimp genome. There are ~200,000 total ERV's in the chimp genome. Those are the facts. Please deal with them.

I have seen some bad homology arguments before but this one gets worse as it goes.

So says the person who thinks 200 out of 200,000 is abundant.

You left out the null hypothesis,

No, I didn't. The null hypothesis is a lack of orthologous ERV's between humans and chimps.

Anyway, you are throwing words around without ever bothering to say what they actually mean. It would not be so bad it you did not do it so often.
The term orthologous segment is defined as a set of genomic segments in different organisms descended from a common ancestor without large rearrangements (Dewey et al., 2006).​
That is classic circular reasoning, it is from a common ancestor so if we find it in the sequence it proves common ancestry. The fact of the matter is that they are called orthologous because they are so much alike, it's as simple as that. You would not find them at orthologous locations because if they were significantly different they wouldn't be called orthologous. Your being fallacious.

Common ancestry is so well evidenced it is assumed as fact. Orthologous sections can still be determined without assuming common descent. All you need to do is align the genomes using very basic alignment tools. No common ancestry assumed, and no circular reasoning.

I could also put it another way. Take 1,000 bases on either side of an ERV said to be orthologous between humans and chimps. Use these 1,000 bases to query the other genome. Guess what you will find? You will find that the DNA flanking the ERV's in either genome are the best fits throughout the genome. This is the test. No circular reasoning needed.

They were compared dude, just like indels in comparative genomics don't have to be the result of insertions or deletions. Not if the genomes are independently created. They are simply differences and if you want to compare the things that are the same and offer them as proof you have to account for the differences.

Evolution doesn't account for differences between species? What have you been smoking?

We are not talking about fingerprints, we are talking about sequences that are prone to mutations.

We are talking about fingerprints. We are talking about the fingerprints of retroviral insertion. We are comparing those fingerprints between genomes. We observe that retroviruses insert into genomes just like we observe that fingers produce fingerprints. You want to ignore the obvious observed mechanism and replace it with a supernatural mechanism that no one has ever observed. That is why I keep comparing your argument to leprechauns planting fingerprints at crime scenes. It is one in the same argument.

You are talking about fragments in a lot of cases and pretending they are all broken in the same place, that's really shallow. What is worse is that you are so short on particulars.

Talk about short on particulars. Take a look at what you wrote.


This one is refreshingly honest:
Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists. Yohn et al, 2005

That is exactly what I have been saying all along. From the species distribution alone one can predict that they will not be found at orthologous positions, and they are not. If PtERV1 insertions were found at orthologous positions in the species they are currently found then this would be a big problem for my argument.


I understand that you are very clumsy with the facts and vague with your terminology. I understand something about evolution you don't, the fact of the matter it is used in at least two different ways at the same time, a fallacy known as equivocation.

More empty assertions.

Not appear, but are orthologous, meaning the sequences are the same.

Orthologous does not mean that the sequences are identical. It means that they are in the same spot in the genome. This is determined by alignments of the two genomes. Like I mentioned earlier, you can take 1,000 bases on either side of an orthologous ERV shared by humans and chimps and do a BLAST search. You will find that the flanking human sequence will find the chimp flanking sequence of the same ERV. No common ancestry assumed.

Do you agree that it's 8% at least?.

Yes. I agree that the estimates from limited data in previous papers were wrong. Of course, they were estimates so they were always going to be wrong. The human genome paper is the definitive source being that they sequenced over 98% of the genome (if memory serves) with quality sequence.

Will you also agree that my argument has nothing to do with the percentage of the genome taken up by ERV's? That it never did? That your whinging about percentages never had anything to do with the argument?
 
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