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Why not? Common features would come with the territory.Now that is a stretch, and it wouldn't explain the hierarchy of commonality.
Right, but there would be no strict hierarchy. Remember that the strong evidence in support of common ancestry is that every ERV that exists in humans and gorillas also exists in chimpanzees, every ERV that exists in humans and orangutans also exists in chimpanzees and gorillas, and so on and so forth.Why not? Common features would come with the territory.
Oh wait, I didn't realize that they were probable ongoing endogenization processes, that explains everything. That would in fact make them human specific, polymorphic and recently active, why didn't I see it before. I must have missed the point where you had got to the point of this.
They don't even coincide in human populations except for framents, those LTRs as they are called.
You have got to be putting me on, these are highly transposable elements, thats how I explain it.
You can conclude no such thing, what it demonstrates is the transposable elements are not consistant even in recent ones. The older ones are riddled with deletions, frameshifts and polymorphisms. You are rumaging through framentary evidence making bold sweeping generalities about things you know nothing about.
How would mitochondrial DNA have any effect whatsoever on ERV's? And why would they enforce a strict hierarchy of commonality?
Firstly, I will admit that I am quite unsure how the process of transposition takes place in a transposable element, although I am aware of the basic mechanisms (mainly reverse transcription for ERVs). This is because the paper fundamentally describes transposition as a populational, not individual, genomic activity (and by the way, notes that no HERVs are being transposed). I'm awaiting some clarification from any of those more knowledgeable in genetics here.
I have no idea what you're trying to say here. Let's look at the quote again:
No current transposition activity of HERVs or endogenization of human exogenous retroviruses has been documented so far.Although unlikely, the continuation of such events in our species cannot be completely excluded per se, because examples of probable ongoing endogenization processes are known from other mammals. For example, mouse mammary tumor virus (MMTV) and murine leukemia viruses in mice, Jaagsiekte sheep retrovirus (JSRV) in sheep, porcine endogenous retroviruses (PERV) in pigs, avian leukemia viruses (ALV) in chicken, and feline leukemia virus (FeLV) in cats have presently both endogenous and exogenous strains (11). Moreover, several of the known class II HERV-K proviruses are human specific and a few loci are polymorphic, indicating very recent activity in evolutionary terms (7, 12).
Let's parse this into a mark-friendly list of points.
1. No HERVs are transposing at present.
2. No HERVs are being endogenized at present.
3. However, we cannot be 100% conclusive about this, because we have seen transposition and endogenization happening in:
3a. mice - MMTV and murine leukemia
3b. sheep - JSRV
3c. pigs - PERV
3d. chicken - ALV
3e. cats - FeLV
3. as evidenced by the fact that both endo- and exogenous strains are present.
4. Moreover, several class II HERV-K proviruses are human-specific
5. and a few loci are polymorphic,
6. showing that they were recently active in evolutionary terms.
Compare again with what you tried to say:
I didn't realize that they were probable ongoing endogenization processes, that explains everything. That would in fact make them human specific, polymorphic and recently active, why didn't I see it before.
1. The paper or this paragraph nowhere implies that any endogenizations are currently occurring in human populations.
2. The paper only states that several class II HERV-K proviruses are human-specific. None of the HERVs Chalnoth cited are human-specific.
3. The paper only states that a few loci are polymorphic.
4. The paper only states that several class II HERV-K proviruses were recently active. None of the HERVs Chalnoth cited were recently active, AFAIK.
Not only did you manage to completely misinterpret the paper, you misinterpreted the very statements which have almost nothing to do with ERV phylogeny.
Mark (#243) : We also know that ERVs are different for different ethnic groups of humans, some that are common in one group is rare in another. How do you explain that?
Me (#245) : Saying that HERV-K is variable hence ERVs are different for different ethnic groups of humans is a little like saying Kent Hovind dislikes the IRS therefore all creationists are felons.
You did not qualify that you only meant HERV-K elements. Can I take this as a concession that the issue of variability across ethnic lines does not occur with any HERVs besides HERV-K?
Mark (#252) : You have got to be putting me on, these are highly transposable elements, thats how I explain it.
But that was not how you explained it yesterday, less than 36 hours ago. Why are your arguments so variable?
Of course recent transposable elements are not consistent across the human genome as they have only been recently endogenized, they haven't "settled down" in a sense, still actively expressed and mutated. But that's a complete red herring, AFAIK the ERVs which vary ethnically are simply not the ones used for phylogenetic analysis and therefore that whole counterargument is wrong.
It seems to me, the basic problem here is that certain traces are found, that show us that a virus was present in the past, like a signature. No?Right, but there would be no strict hierarchy. Remember that the strong evidence in support of common ancestry is that every ERV that exists in humans and gorillas also exists in chimpanzees, every ERV that exists in humans and orangutans also exists in chimpanzees and gorillas, and so on and so forth.
Yes, all creationist ideas may explain some degree of similarity between various species. But they don't explain a strict hierarchy. Evolution, on the other hand, explains it perfectly: at one point, these disparate species were one species. They became separated geographically, and, in time, diverged in their evolution to the point they could no longer mate. Thus some changes occurred in the parent species, and some changes occurred after the speciation event. The changes that occur in the parent species will exist in all child species.
Need I really say more Mark? You accuse others of dropping out of the discussion, while you yourself walk away from it. If there is another definition of hypocricy, I'm all ears. But your behavior comes pretty close.That's it!? All you have is a childish insult when the topic is ERVs? For one thing I'm immune to your venom and for another I know that an ad hominem approach to discussion on here is a logical fallacy. I allways know when it's time to move on to another topic when thats all the evolutionists on here have left.
Have a nice day
Need I really say more Mark? You accuse others of dropping out of the discussion, while you yourself walk away from it. If there is another definition of hypocricy, I'm all ears. But your behavior comes pretty close.
Right, that resesarch was done back in 1981. Also, you yourself have bemoaned the use of genetic clocks as being uncertain. There is a good deal of uncertainty involved in using genetic drift of mitochondrial DNA built a phylogenic tree.They don't use ERVs to establish taxonomic catagories, the taxonomy of ERVs is itself a source of confusion. They use mtDNA and they have been doing it for a long time, it is a well established but controversial hierarchy building measurement. This is what they found when comparing chimps, gorrillas and humans:
"The high rate of evolution of mitochondrial DNA makes this molecule suitable for genealogical research on such closely related species as humans and apes. Because previous approaches failed to establish the branching order of the lineages leading to humans, gorillas, and chimpanzees, we compared human mitochondrial DNA to mitochondrial DNA from five species of ape (common chimpanzee, pygmy chimpanzee, gorilla, orangutan, and gibbon). About 50 restriction endonuclease cleavage sites were mapped in each mitochondrial DNA, and the six maps were aligned with respect to 11 invariant positions. Differences among the maps were evident at 121 positions. Both conserved and variable sites are widely dispersed in the mitochondrial genome. Besides site differences, ascribed to point mutations, there is evidence for one rearrangement: the gorilla map is shorter than the others owing to the deletion of 95 base pairs near the origin of replication. The parsimony method of deriving all six maps from a common ancestor produced a genealogical tree in which the common and pygmy chimpanzee maps are the most closely related pair; the closest relative of this pair is the gorilla map; most closely related to this trio is the human map. This tree is only slightly more parsimonious than some alternative trees. Although this study has given a magnified view of the genetic differences among humans and apes, the possibility of a three-way split among the lineages leading to humans, gorillas, and chimpanzees still deserves serious consideration. "Evolutionary Tree for Apes and Humans Based on Cleavage Maps of Mitochondrial DNA
The split between chimpanzees and humans was supposed to have come after the split between the common ancestor and gorrillas.
So what? They're suggesting cross-species transfers of ERV's. That's not a problem in the least for the argument for ERV's as tracers of common ancestry. First of all, these ERV's will exist in different locations in the genome. Second of all, it still doesn't destroy the probabilistic argument I've been using one iota, because this would be a mode of transfer that would be completely unrelated to the phylogenic tree, and thus we would not expect a tree structure if the ERV's we are studying had such parallel transmission.What the mtDNA should be showing is that we are more like the chimpanzee then the gorrilla but it isn't doing that. Now I want you to pay attention here because this is very important. There is a line of evidence that meets the Talk Origins standard for falsification:
"Two larger gammaretrovirus-like groups (PtG1 and PtG2) occurred in chimpanzees but not in humans. The PtG sequences were most similar to two baboon ERVs and a macaque sequence but neither to other chimpanzee ERVs nor to any human gammaretrovirus-like ERVs."Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees
Please, if you think you have anything that can disprove ERVs as tracers of common ancestry, go ahead and post it. But to do so, you're going to need to find a mechanism that enforces a strict hierarchy in commonality when no common ancestry exists.I didn't want to get into this and I still don't, however, if this arguement keeps coming up I will. You might want to think about that because these homology arguements do not stand up when critically examined.
Think carefully about where this is going and I will check the thread later for your response.
Consider:It seems to me, the basic problem here is that certain traces are found, that show us that a virus was present in the past, like a signature. No?
Where the similarities are very great, like chimps and humans they say there was a common ancestor. Or, wicked pre flood people having offspring could account for it. If we want to talk other apes, or monkeys, that have some traces, and shared some virius, then we may simply look at not offspring, but shared virus in the different past. Somewhat like aids, today. I think that covers the whole thing here, anything missing??
There is only one ERV still active, it's the HERV-K virus if that's what you mean. The rest are marked by LTRs which are supposed to be the smoking gun here because they supposedly can't get rid of them.
The HERV-K proviruses still have a few loci that are polymorphic. These ERV families are nearly extinct in our genome with that one exception.
The ones that are not polymorphic are fragmented by mutations, that is how their reading frames were shut down. If you had a reasonably good point then I must have missed it.
Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10254-60.
Constructing primate phylogenies from ancient retrovirus sequences.
Department of Molecular Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA.
The genomes of modern humans are riddled with thousands of endogenous retroviruses (HERVs), the proviral remnants of ancient viral infections of the primate lineage. Most HERVs are nonfunctional, selectively neutral loci. This fact, coupled with their sheer abundance in primate genomes, makes HERVs ideal for exploitation as phylogenetic markers. Endogenous retroviruses (ERVs) provide phylogenetic information in two ways: (i) by comparison of integration site polymorphism and (ii) by orthologous comparison of evolving, proviral, nucleotide sequence. In this study, trees are constructed with the noncoding long terminal repeats (LTRs) of several ERV loci. Because the two LTRs of an ERV are identical at the time of integration but evolve independently, each ERV locus can provide two estimates of species phylogeny based on molecular evolution of the same ancestral sequence. Moreover, tree topology is highly sensitive to conversion events, allowing for easy detection of sequences involved in recombination as well as correction for such events. Although other animal species are rich in ERV sequences, the specific use of HERVs in this study allows comparison of trees to a well established phylogenetic standard, that of the Old World primates. HERVs, and by extension the ERVs of other species, constitute a unique and plentiful resource for studying the evolutionary history of the Retroviridae and their animal hosts. emphasis mine
Well, I would think that was possible, if the similarities were great there as well. But if it is less of a similarity, I would lean to the transfer of virus between species.Consider:
There are ERV similarities between humans, chimpanzees, and gorillas. Your 'theory' suggests that people mated with gorillas as well as chimpanzees.
Great, so are you suggesting some limit for wicked pre flood man in that department? If apes fit the bill, thenhey, let's go with the evidence.Thus one of the predictions of your 'theory' would be that some ERV's would be in common between humans and gorillas, but not chimpanzees. In reality, this never happens: any similarity between humans and gorillas is also shared by chimpanzees.
Well, I would think that was possible, if the similarities were great there as well. But if it is less of a similarity, I would lean to the transfer of virus between species.
Retroviruses insert randomly into the genome among thousands of possible insertion sites. Let's say that there are 5,000 possible insertion sites for a virus, a very conservative number. That would mean that the chances of two individuals sharing the same insertion is 1 in 5,000. In the case of primates, there are dozens and dozens of shared insertions. The chances of sharing 20 insertions, by separate chance infections, is 1 in 5,000^20, or 1 in 9.53674316 × 10^73
Great, so are you suggesting some limit for wicked pre flood man in that department? If apes fit the bill, thenhey, let's go with the evidence.
Actually, common ancestry fits the bill.
Need I really say more Mark? You accuse others of dropping out of the discussion, while you yourself walk away from it. If there is another definition of hypocricy, I'm all ears. But your behavior comes pretty close.
It is difficult to get rid of any insertion, either through primary infection or transposition of the element. That is the whole point.
Here is a very simple question. Were you born with zero HERV's, or did you inherit your HERV's from your parents?
And how do we know that HERV-K is still active?
Because there are human-lineage specific insertions.
How do we know that other ERV families are no longer active?
Because there are no human-lineage specific insertions of that family.
If you claim that HERV-K is still active then you must admit that the common ancestry model is accurate.
The point is that a comparison of mutations within ERV's also forms a phylogenetic tree, the same one that the pattern of insertions produces. Stunning, isn't it? These mutations that you speak of is actually one more piece of evidence supporting common ancestry. Here is the abstract:
Now when the HERV's articles are talking about ORF's what is their point?Regions of DNA that encode proteins are first transcribed into messenger RNA and then translated into protein. By examining the DNA sequence alone we can determine the sequence of amino acids that will appear in the final protein. In translation codons of three nucleotides determine which amino acid will be added next in the growing protein chain. It is important then to decide which nucleotide to start translation, and when to stop, this is called an open reading frame.
Once a gene has been sequenced it is important to determine the correct open reading frame (ORF). Every region of DNA has six possible reading frames, three in each direction. The reading frame that is used determines which amino acids will be encoded by a gene. Typically only one reading frame is used in translating a gene (in eukaryotes), and this is often the longest open reading frame. Once the open reading frame is known the DNA sequence can be translated into its corresponding amino acid sequence. An open reading frame starts with an atg (Met) in most species and ends with a stop codon (taa, tag or tga).
the point is that there has not been mutations that involve stop codons that "break" the proteins being made from these genes.HERV-K113
was found to have full-length open reading frames (ORFs)
for all viral proteins, with no substitutions that would alter
amino acid sequence motifs that are well conserved
among retroviruses.
they have found HERV-K's in some human populations and not others, the infection occurred after the human populations began to migrate away from each other. After those populations WERE human. That is what it means to be extinct, not active currently in human populations.And how do we know that HERV-K is still active? Because there are human-lineage specific insertions. How do we know that other ERV families are no longer active? Because there are no human-lineage specific insertions of that family. If you claim that HERV-K is still active then you must admit that the common ancestry model is accurate.
so the extinction issue revolves around poliferation and fixation in a population, it has nothing to do with ORF.The extinction of this family apparently was not a consequence of its slow gradual degeneration, but the outcome of the fixation of specific restrictive alleles in the human-chimpanzee ancestral population. Three species-specific insertions (two in humans and one in chimpanzees) were identified, further supporting that extinction took place when these two species were beginning to diverge. These are the only fixed differences of this kind so far observed between humans and chimpanzees, apart from those belonging to the human endogenous retrovirus K family.
Thus, all humans share virtually the same array of TE insertions, which date back to the distant past of our evolutionary lineage, so that we also share many TE sites with the other Hominoidea (gibbons, orangutans, gorillas, and chimpanzees). The reasons for these differences are not completely understood, but they probably stem from both the smaller effective population size of mammals than of insects and the involvement of ectopic exchanges in the selective control of TE copy numbers
TE=transposable element
...
Not the least important of them is what stops the invasion process of a genome by a TE family. The sequenced human genome, harboring thousands of copies from TE families that became "extinct" when they lost their capacity of proliferation, offers an exceptional opportunity to investigate this problem.
...
The human genome harbors nearly half a million copies of roughly 100 HERV families (25). All of these families, except one, are now apparently extinct, i.e., they can spread no further over the genome. The only exception is HERV-K, which has three human-specific subfamilies (8), some of whose insertions are polymorphic in modern human populations and thus may still be capable of movement (42). The ultimate cause of the extinction of a TE family will be the reduction of its proliferation rate below a certain threshold, which depends on the per-nucleotide mutation rate.
from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1448813The oldest L1 elements in the genome have accumulated deleterious mutations that render them inactive. However, younger L1 elements have been identified that remain actively mobile today (Moran et al. 1996; Brouha et al. 2003). These active copies contain two intact open reading frames, ORF1 and ORF2, which encode proteins that are necessary for L1 retrotransposition (Feng et al. 1996; Moran et al. 1996). ORF1 encodes a 40-kD protein with RNA-binding activity (Hohjoh and Singer 1996, 1997a,b; Kolosha and Martin 1997; Martin et al. 2000, 2003; Martin and Bushman 2001), whereas ORF2 encodes a protein with both endonuclease (EN) and reverse transcriptase (RT) activities
Right, that resesarch was done back in 1981. Also, you yourself have bemoaned the use of genetic clocks as being uncertain. There is a good deal of uncertainty involved in using genetic drift of mitochondrial DNA built a phylogenic tree.
The ERV method is vastly better, because there are far fewer uncertainties involved. It is much, much harder for an ERV to do anything other than follow the phylogenic tree exactly.
So what? They're suggesting cross-species transfers of ERV's. That's not a problem in the least for the argument for ERV's as tracers of common ancestry. First of all, these ERV's will exist in different locations in the genome. Second of all, it still doesn't destroy the probabilistic argument I've been using one iota, because this would be a mode of transfer that would be completely unrelated to the phylogenic tree, and thus we would not expect a tree structure if the ERV's we are studying had such parallel transmission.
Please, if you think you have anything that can disprove ERVs as tracers of common ancestry, go ahead and post it. But to do so, you're going to need to find a mechanism that enforces a strict hierarchy in commonality when no common ancestry exists.
Not in the least. The average divergence between humans and chimpanzees, as far as base pair substitution is concerned, is only 1.23%. Do you really think that ERV's would be unrecognizable with only an average divergence of 1.23%?The only HERV left still active in the human genome is HERV-K. The rest are fragments and the longest one I have seen is around 7 thousand base pairs. You are talking about framents that are riddled with all kinds of mutations, making a genuine arguement for common ancestry is hopelessly probablematic.
I'm not addressing the evidence that you are presenting because I don't think it has any relevance to the discussion. It seems to me that you are attempting to cast doubt upon the usability of ERV's as tracers of common descent because they tend to copy themselves to other places in the genome.Twice I elaborated at lenth on the current research being done and twice you completly ignored it. Now if you are going to talk in circles around the actual evidence then I will find something more productive to to with my time. What are your sources for making this sweeping statement and what is the evidence involved?
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