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

Zaius137

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About my Haldane turnoff… You don’t’ have to even talk about it. I thought you might want to go down that road. I have on purpose occasionally asked a question I know you have no answer for. So just let it go.

“Also wrong. They should share the insertion point only if their common ancestor was infected with the virus and an insertion occurred in that population. Instead, the descendents were infected and therefore should not share insertion points.”

That works for my argument that chimps and humans do not share a common ancestor. Your argument is not doing so well…

Look… gorillas and chimps supposedly diverged before human and chimps according to the tale. Infection in the great ape line shows up in the chimps; chimps and great apes diverged according to the tale then humans diverged threw a common ancestor from the chimps according to the tale. The infection should show up in orthologous loci in the human line… it shows up in gorilla and chimpanzee genomes but not in the human loci. Gorilla then chimp and human. It is found in the Gorilla but not the human… hence it is missing and anomalous.

“You never see substantial arguments because you don't understand the issues.”

You use this phrase a lot but I have always been able to maintain my point with you.

The odds are in my favor… shameless dig. But maybe you have a real point to make in your next reply.
 
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Naraoia

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To Naraoia…

“If only one ERV is allowed to undergo fixation at a time, which is bullcrap. Just how many polymorphisms exist in the human gene pool right now? You seem to have a persistent problem with parallel vs. sequential trials.”

How is that bullcrap??? You need to explain how more fixations can happen under neutral selection (non coding HERV’s). Suggestions like Synergistic epistasis need a selective agent.
Think about it, for heaven's sake. What law of nature forbids more than one neutral polymorphism from existing simultaneously in a population? (Hint: none.) And what happens to neutral polymorphisms eventually? (Hint: they drift to fixation.)

Now add those two together...

(Synergistic epistasis? Where on earth did that come from?)

I think "up to" 280 times is a lot less than you need to kick this particular p-value into non-significance...
Our last go around with probability was frustrating for me… I am not sure your suit is probability.
Well, I wasn't the one who confused possible values of a random variable with expectations :p

Sorry I did not get to these earlier…Nothing I can really say about your responses not lining up with what I said.
*Zaius waves his hands and the problem... doesn't go away*

It is just not consistent with the documentation I looked at. Try and read the following…as the famous line goes “The problem here... is a failure... to communicate”.
The problem here was your misreading of Yohn et al. 2005. I'm trying to communicate...

The author assumes that the only reason that chimpanzees and gorillas, but not humans, would share an ERV insertion is that it inserted twice. He seems not to have heard of incomplete lineage sorting, or be aware that it is well known that chimps and gorillas are more closely related to each other than to humans in about one-sixth of their genome. (The same is true for humans and gorillas; humans and chimpanzees are only most closely related, genetically speaking, in two-thirds of their genome.)
Hmm, that's good to know.

Yohn et al are talking about a retrovirus that infected both African great apes and Old World monkeys, but not humans. It is not talking about identical insertion points in great apes and monkeys, which really would be a strong piece of evidence against ERVs as markers of common descent. In fact, the paper sets a lower bound of 95.8% on the fraction of shared insertion sites. Did the the author not read the paper in question (or even the entire abstract, since the 95.8% number is there)? Is he simply clueless about the subject he's writing about?

I guess this is the best creationists can do.
So it wasn't even Zaius who misread the paper. Creationist misunderstandings are contagious, it would seem.

It does not matter where or how often the insertions take place. To be fixed in a population Haldane is very clear about the 300 generations per insertion.
Incidentally, I was under the impression that the fixation time of a neutral mutation is proportional to effective population size, it's not some fixed number.

You missed my point about neutral selection all together.
So long as you keep seriously talking about "neutral selection", it's unlikely that you have a point...

Yes the point is that the ERV (HERV-k) is in the great apes and the chimps but not in humans.
What does the H in HERV-K stand for? ;) You meant PtERV-1, I think.

If the human and chimp were common ancestors the insertion (since it is in the apes today) should be in humans… it is not.
The point is that the chimp and gorilla insertions are not in the same place. Hence they are not orthologous insertions. That is, chimps and gorillas did not inherit them from their common ancestor. Ergo, they need not be present in humans.
 
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Zaius137

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I know you can not grasp my point so here is a reply from the author of the article that was being criticized. At least He found this criticism important enough to reply to.

“Since [HERV-K-GC1] is an unrepresentative deviation from a pattern, all that needs to be done is identify mechanisms that can account for that deviation. There are at least two known mechanisms to account for it (Barbulescu et al., 2001):

Here they are...

“The insertion was in an allele that remained heterozygous in the populations across two divergences, given genetic drift and the divergent sub-population size (allelic segregation).”

I like this tap-dance because now an allele can be suggested. Sorry evolutionist you can’t have your cake and eat it too. Yes Haldane’s dilemma does not claim neutral selection in fixing a gene into a population. But if the author can claim that this gene is in an allele (no reason why it can’t be coding and under selection) then Haldane’s 300T is in full force. Isn’t it nice when things just fall together?


“The insertion was in a duplicate section of the chromosome that underwent homologous recombination in each respective linage.”


OOPs remember this locus was intact. Three similar homologous recombination’s in divergent species? Why didn’t he just say that God did it (the real fact of the matter).

No score for the author…

http://www.evolutionarymodel.com/evolutionnews.htm


You know that I can not agree with the identification of supposed EVRs in the human genome. After the chimp genome is butchered by the algorithms how can real associations be made in the loci of mythical ERV infections. Remember 200 thousand were supposedly identified but only 9 occurred after the chimp human split…


You have ~9 insertions of ERVs since the supposed spit of chimps and humans (unique to humans) that was supposed to be 6 million years. Now there are supposedly 200 thousand ERV insertions in the human genome overall (International Human Genome Sequencing Consortium, 2001). If ~ 9 insertions normalized in our population in 6 million years how in the heck did 200 thousand insertions happening in vertebrates in 100 million years? 9/6m=x/100m… that only equals 150 insertions how do you get to 200 thousand. Evolutionists are nuts…
 
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Huram Abi

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If ~ 9 insertions normalized in our population in 6 million years how in the heck did 200 thousand insertions happening in vertebrates in 100 million years? 9/6m=x/100m… that only equals 150 insertions how do you get to 200 thousand. Evolutionists are nuts…

9/6,000,000=.0000015

200,000/100,000,000=.0000020

So we are talking about 0.00015% rate of insertion verses 0.00020%

There is no reason to expect the rate to be a k constant and the minute deviation between these two rates is so negligible it is immaterial.

Nominal values don't tell us nearly as much as ratios.
 
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sfs

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About my Haldane turnoff… You don’t’ have to even talk about it. I thought you might want to go down that road. I have on purpose occasionally asked a question I know you have no answer for. So just let it go.

I might want to go down what road? You've made a clearly false claim, that Haldane's argument applies to neutrally evolving alleles.
You can try to ignore it, but there's no changing the fact that you blew it.

“Also wrong. They should share the insertion point only if their common ancestor was infected with the virus and an insertion occurred in that population. Instead, the descendents were infected and therefore should not share insertion points.”

That works for my argument that chimps and humans do not share a common ancestor. Your argument is not doing so well…

Look… gorillas and chimps supposedly diverged before human and chimps according to the tale. Infection in the great ape line shows up in the chimps; chimps and great apes diverged according to the tale then humans diverged threw a common ancestor from the chimps according to the tale. The infection should show up in orthologous loci in the human line… it shows up in gorilla and chimpanzee genomes but not in the human loci. Gorilla then chimp and human. It is found in the Gorilla but not the human… hence it is missing and anomalous.
Are you not aware that the same virus can infect more than one species? Viruses cross between species all the time -- just look at HIV, or flu. So the mere fact that two species were infected with closely related viruses tells us nothing about their phylogeny. ERV insertion points, on the other, are changes to the organism's DNA, and so they are passed on to descendents, and so they should provide evidence about phylogeny. Really, it would help if you could figure out what the argument was about.

“You never see substantial arguments because you don't understand the issues.”

You use this phrase a lot but I have always been able to maintain my point with you.
Precisely my point: you think you're maintaining your side of the argument well, even while making egregiously wrong statements -- as you have here about Haldane and neutral evolution, and about shared infection being a phylogenetic marker. You simply do not know enough genetics or statistics to know when you're on target and when you're shooting yourself in the foot.
 
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Huram Abi

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To Humram Abi

9/6,000,000=.0000015 ?

I got 9/6000000 = .000002 I think you have a broken calculator.

No I am not maintaining a k value here but only similar mechanisms should at least produce a answer within an order of 10….


uh... try 9/600=.015

Your calculator is rounding up.... to the exact same ratio as 200,000/100,000,000.

The deviation is so negligible, your calculator isn't even able to compute a distinction between the two ratios.
 
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pgp_protector

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To Humram Abi

9/6,000,000=.0000015 ?

I got 9/6000000 = .000002 I think you have a broken calculator.

No I am not maintaining a k value here but only similar mechanisms should at least produce a answer within an order of 10….

I think it's your calculator that is broken.
.000002 * 6000000 = 12 not 9 :)
.0000015 * 6000000 =9
 
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sfs

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I know you can not grasp my point so here is a reply from the author of the article that was being criticized. At least He found this criticism important enough to reply to.

“Since [HERV-K-GC1] is an unrepresentative deviation from a pattern, all that needs to be done is identify mechanisms that can account for that deviation. There are at least two known mechanisms to account for it (Barbulescuet al., 2001):

]Here they are...

“The insertion was in an allele that remained heterozygous in the populations across two divergences, given genetic drift and the divergent sub-population size (allelic segregation).”
Everything is fine up to here. The suggested mechanism is the one I already mentioned, incomplete lineage sorting. Is there any reason to think this didn't happen? Did the author give you any reason?

Now this -- is this you, or are you quoting the author of the article? (And how did you get this reply? Did you email him?)

I like this tap-dance because now an allele can be suggested. Sorry evolutionist you can’t have your cake and eat it too. Yes Haldane’s dilemma does not claim neutral selection in fixing a gene into a population. But if the author can claim that this gene is in an allele (no reason why it can’t be coding and under selection) then Haldane’s 300T is in full force. Isn’t it nice when things just fall together?
This paragraph has no meaning that I can figure out. It certainly makes no genetic sense.

“The insertion was in a duplicate section of the chromosome that underwent homologous recombination in each respective linage.”
Why don't we just stick with the one mechanism, incomplete lineage sorting? We know it should happen, we can see that it has happened in about 1/8th of human/chimpanzee/gorilla differences (not 1/6th as I thought). So what's the problem with it? Didn't the author have any rebuttal?

You know that I can not agree with the identification of supposed EVRs in the human genome. After the chimp genome is butchered by the algorithms how can real associations be made in the loci of mythical ERV infections. Remember 200 thousand were supposedly identified but only 9 occurred after the chimp human split…
Why would you expect transposition rates to be constant across hundreds of millions of years, since the organisms involved are quite different and have different population structures?
 
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Zaius137

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“Everything is fine up to here. The suggested mechanism is the one I already mentioned, incomplete lineage sorting. Is there any reason to think this didn't happen? Did the author give you any reason?”

If the author or you can make such bold suggestions why can’t I say that the allele is under mild selection if not total selection if the insertion damaged it. Speculation is a two edged sword. Haldane’s dilemma is in full force because if the insertion took place in an allele under selection the insertion is under selection… period.

Now this -- is this you, or are you quoting the author of the article? (And how did you get this reply? Did you email him?)

I am but a simple layperson why would he even let me shine his shoes. The reply was in the citation. Here it is again.

http://www.evolutionarymodel.com/evolutionnews.htm

“Why don't we just stick with the one mechanism, incomplete lineage sorting? We know it should happen, we can see that it has happened in about 1/8th of human/chimpanzee/gorilla differences (not 1/6th as I thought). So what's the problem with it? Didn't the author have any rebuttal?”

Because it was his rebuttal… read the citation. Unless you want to argue with a fellow evolutionist over may point?


“Why would you expect transposition rates to be constant across hundreds of millions of years, since the organisms involved are quite different and have different population structures?

Because evolutionists do…. Hence the paleovirology nonsense.” I believe in the Biblical creation not evolution magic.


 
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sfs

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“Everything is fine up to here. The suggested mechanism is the one I already mentioned, incomplete lineage sorting. Is there any reason to think this didn't happen? Did the author give you any reason?”

If the author or you can make such bold suggestions
Neither of us have made any bold suggestions.
why can’t I say that the allele is under mild selection if not total selection if the insertion damaged it. Speculation is a two edged sword. Haldane’s dilemma is in full force because if the insertion took place in an allele under selection the insertion is under selection… period.
If the mutation were deleterious, as you suggest, then Haldane's model still has nothing to do with the situation; it would not have fixed in any population in that case.

Now this -- is this you, or are you quoting the author of the article? (And how did you get this reply? Did you email him?)

I am but a simple layperson why would he even let me shine his shoes. The reply was in the citation. Here it is again.

http://www.evolutionarymodel.com/evolutionnews.htm
Ah, I didn't see that citation. So you already have a lengthy, detailed response explaining why Jonathan M's article was bunk. So why are we discussing this?

“Why would you expect transposition rates to be constant across hundreds of millions of years, since the organisms involved are quite different and have different population structures?

Because evolutionists do….
They do? Where?
 
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Zaius137

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(sfs)…

“If the mutation were deleterious, as you suggest, then Haldane's model still has nothing to do with the situation; it would not have fixed in any population in that case.”

My point would be that these insertions were not necessarily neutral… OK. Remember I am unconvinced of these ridiculous scenarios. Common ancestry, time of divergence and paleovirology is complete nonsense to me and involves these contrived un-parsimonious explanations. There is so many problems with this evolution pseudoscience it is hard to keep the fantasy straight.

“Why would you expect transposition rates to be constant across hundreds of millions of years, since the organisms involved are quite different and have different population structures?

Because evolutionists do….

They do? Where?”

The rest of my quote….Because evolutionists do…. Hence the paleovirology nonsense.” I believe in the Biblical creation not evolution magic.
 
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Zaius137

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I speak to a lot to professional Christians (scientists) about why some of them can buy into this evolution dogma. It seems the saddest thing to me that a Christian can believe this evolution story of origins that has no power to explain the origin of life in the first place. If God created life why can’t he create the species also? Species need not to arise by some unsupportable speculation.
 
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Aeneas

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I speak to a lot to professional Christians (scientists) about why some of them can buy into this evolution dogma. It seems the saddest thing to me that a Christian can believe this evolution story of origins that has no power to explain the origin of life in the first place. If God created life why can’t he create the species also? Species need not to arise by some unsupportable speculation.

And scientists think it just as sad that some people confuse abiogenesis and evolution and pretend that the validity of one impacts the other.
 
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sfs

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(sfs)…

“If the mutation were deleterious, as you suggest, then Haldane's model still has nothing to do with the situation; it would not have fixed in any population in that case.”

My point would be that these insertions were not necessarily neutral…
And my point is that insertions are marks of phylogeny regardless of their selective value.

OK. Remember I am unconvinced of these ridiculous scenarios.
Common ancestry, time of divergence and paleovirology is complete nonsense to me and involves these contrived un-parsimonious explanations. There is so many problems with this evolution pseudoscience it is hard to keep the fantasy straight.
I do remember that, and I also remember that you have been unable to offer any coherent reason for your rejection, nor for thinking that these are unparsimonious explanations.

“Why would you expect transposition rates to be constant across hundreds of millions of years, since the organisms involved are quite different and have different population structures?

Because evolutionists do….
They do? Where?”

The rest of my quote….Because evolutionists do…. Hence the paleovirology nonsense.” I believe in the Biblical creation not evolution magic.
"Hence the paleovirology nonsense" is not a place where evolutionary biologists have expressed an expectation that transposition rates have been constant over hundreds of millions of years. Now, could you answer the question?
 
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Loudmouth

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I suppose you mean orthologous. Actually out of the tens of thousands of supposed ERV insertion in humans about 12 are shared with the apes and were located by algorithms.


False. Over 200,000 are shared between humans and apes. This is discussed in the OP's essay. Only a relative handful are not shared by humans and chimps, and an even smaller number do not fit the expected phylogeny due to allele sorting at the chimp/gorilla split.

Since there are literally tens of thousands of these insertions that must be fixed into the human population lets look at how long that would take according to Haldane and his 300T generations. In humans with about 20 years per generation and 300 generations that gives about 6000 years per single insertion. Now a conservative estimate of 10 thousand insertion sites gives 10k times 6k which equals about 60 million years between the common ancestor of apes and humans. That figure is ten times the supposed divergence time.

The vast majority of the 200,000 ERV's would have already been fixed in the common ancestor. You do realize this, do you not? You and your siblings share 200,000 ERV's at the same location in each genome. Are you suggesting that all 200,000 ERV's became fixed in a single generation? Are you suggesting that these orthologous ERV's are not due to common ancestry?

Can there be another explanation other than common ancestry. Of course there is; what if the loci of these insertions were highly selective and independent events in humans and apes.

Please cite research that would produce only 1% non-orthologous insertions and 99% orthologous insertions for a given virus. All of the studies I have seen show exactly the opposite, such as this experiment:

Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

“But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to
280 times more frequently than predicted mathematically


So let's look at those odds, using the 280 figure. There are 3 billion bases in the human genome. The 1:1 odds of a virus inserting at any specific base is 1 in 3 billion. If we increase those odds to 280 to 3 billion for a given base that is still a ~1 in 10 million chance of inserting into this preferred site. And that is just for one insertion. The chances of 10 indendent insertions occuring at orthologous positions using your best odds are 1 in 10 million to the 10th power, or 1 in 10^70. Yes, that is 1 with 70 zeros after it. What do you think the odds are for 200,000 ERV's?

Are ERV’s an indication of common decent or common design.

You and your siblings share 200,000 ERV's at the same location in your genomes. Is this due to common ancestry or common design? Are you going to claim that you are your siblings were magically poofed into being with the ERV's already in place?
 
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Loudmouth

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I speak to a lot to professional Christians (scientists) about why some of them can buy into this evolution dogma. It seems the saddest thing to me that a Christian can believe this evolution story of origins that has no power to explain the origin of life in the first place. If God created life why can’t he create the species also? Species need not to arise by some unsupportable speculation.

So you would argue against your own birth? Afterall, if God can create you through magical poofing why rely on biological reproduction?
 
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