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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.
Excuse me but the LTRs 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.
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.
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.
This is the only valid observation you have made so far.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.
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.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:
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% ?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???
As the result of a 5% change, give or takeThe GaG, PoL, and EnG still look like the HERV-K. So your telling me that a ape like hominid changed into a modern human
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.but the HERV-K virus (with an astounding mutation rate) stayed a HERV-K virus.
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.Then that virus mysteriously went extinct 100,000 years ago even thou the human population increased; more hosts more viral infections.
ERVs support evolution. Your incredibly low incredulity threshold is not a yardstick by which we measure reality.If you can still say that ERVs support evolution I can still say you are nuts.
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?
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.
Homology could also put forward common design.
Excuse me but the LTRs 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.
Owing to the retroviral reverse transcription strategy, both LTR sequences are identical in sequence at the time of provirus formation.
Thats from your article Remember the LTRs are removed to produce the phony resurrected virus snip, snip.
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?
Evolution is religion not observable science. You still pay homage to mischievous leprechauns and magic (central to your origin fairytales).
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.
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.
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.
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?
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.
Homology could also put forward common design.
Homology could also put forward common design.
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.
At least you admit that your argument is based on a fallacy, an argument from incredulity.
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.
Hey, Mark --
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.
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.
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.
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,
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.
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.
Common ancestry is untestable and unfalsifiable
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.
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.
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.
Second, retroviral insertions may very well be deleterious. This would lead to selection of mutations such as indels.
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.
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.
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.
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.
There are over 200,000 ERV's in the chimp genome. PtERV insertions make up less than 1% of all ERV's.
Which they shouldn't if evolution is true. That you don't understand that only highlights your ignorance of how evolution works.
Zaius claims just the opposite. You guys need to get together and form a consistent argument.
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 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 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.
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.
You left out the null hypothesis,
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.
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.
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.
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
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.
Not appear, but are orthologous, meaning the sequences are the same.
Do you agree that it's 8% at least?.
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