ERV's: Evidence of Common Ancestory

That's a good example. Nowhere do they tackle the problem of the pattern of homology which is what points to evolution.The aptly named blogger ERV (aka SA Smith) has a great section that deals with the common creationist claims relating to endogenous retroviruses: Index to Common Creationist Claims about ERV'sShe covers the claims dealing with origin, insertion, and function of ERV's in a very concise manner.

There are hundreds of thousands of ERV's in the human genome. Only a handful are not fixed in the population. What Loudmouth was saying was that when the retroviral insertion FIRST happens it will be passed on like any other heterozygous allele. It's somewhat like blood type. If one of your parents has a blood type AB then half of their gametes will carry the A allele and the other half will carry the B allele. For ERV's that have not become homozygous in the population the two alleles are the ERV and the empty insertion site. Like I said above, only a handful out of the hundreds of thousands of ERV's are not fixed in the population.

Theories are never proven. Theories can only be tested. As new evidence comes to light, like ERV's, the theory is tested once again.As for ERV's, the theory of evolution predicts three things. First, ERV's that are shared in the same genomic position must produce the same nested hierarchy that is based on morphology. With very, very few exceptions, this is true. Secondly, the theory of evolution predicts that the divergence of the DNA sequence of the ERV should match the evolutionary distance established by the nested hierarchy. For example, an ERV shared by orangutans, humans, and chimps should vary more than an ERV shared by just humans and chimps. The theory passes this test as well. Thirdly, when an ERV inserts the LTR's (Long Tandem Repeats) that flank the retroviral DNA are exactly the same DNA sequence. After insertion the LTR's will diverge due to the accumulation of mutations. Therefore, the longer that an ERV has been in a lineage the more divergence one should see between the LTR's of the same ERV. This time period established by the LTR's should match the other two pieces of evidence, and it does.IOW, the pattern AND sequence divergence of ERV's is exactly what we should see if evolution is true. With creationism/ID we wouldn't even predict that any two species would share the same codon usage, much less orthologous ERV's. That is the problem here, creationism/ID is incapable of predicting what types of patterns we should see between species which makes the "common designer, common design" claims a bit hollow.Edited by Taq, : No reason given.

I would say that it is the opposite of laziness. It takes effort to purposefully change the sequences of the ERV's so that they produce the same phylogeny as the location of the ERV's. God would have to go to each ERV and change the LTR sequences so that the insertion time derived from the LTR divergence matches the insertion time derived from the loci. God would also have to make sure that the same ERV between species has enough changes so that they too produce the same insertion time derived from the other two methods. This takes some effort.What it argues for is Loki, a god who purposefully tricks his creations.

I get this from the chimp and human genome papers (these are large .pdf's so be warned if you are on dial up).The human genome paper:
http://www.nature.com/...journal/v409/n6822/pdf/409860a0.pdfThe chimp genome paper:
http://www.nature.com/...rnal/v437/n7055/pdf/nature04072.pdfIn Table 11 on pg. 880 of the human genome paper it states that there are 112,000 ERV-class I insetions, 8,000 ERV(K)-class II insertions, and 83,000 ERV(L)-class III insertions for a total of 203,000 ERV's in the human genome.In Table 2 on page 75 of the chimp genome paper it lists the species specific ERV's, those ERV's that are not shared between humans and chimps. Chimps have 279 ERV's that are not found in humans and humans have 82 ERV's not found in chimps. This would mean that the bulk of ERV's found in humans (203,000) are also found in chimps.As for ERV's that are not found in all humans, these are a tiny, tiny minority. I am only aware of a handful of such ERV's, such as this one:

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Neurosci Lett. 2006 Nov 20;408(3):226-9. Epub 2006 Sep 26.

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Insertional polymorphism of endogenous retrovirus HERV-K115 in schizophrenia.

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Otowa T, Tochigi M, Rogers M, Umekage T, Kato N, Sasaki T.

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Department of Neuropsychiatry, Graduate School of Medicine, University of Tokyo, Bunkyo, Tokyo 113-8655, Japan.

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Retroviruses are implicated in the pathogenesis of schizophrenia. Human endogenous retrovirus type K115 (HERV-K115) is a full-length, potentially transcriptional retrovirus and is also polymorphic. We investigated the frequency of HERV-K115 in Japanese schizophrenia patients and healthy controls. No difference was found in the frequency between patients and controls (8.4% versus 9.4%, respectively). However, a marginal difference was observed in age at onset between the HERV-K positive and negative patients (p=0.057). The HERV-K115 insertion appeared to be more frequent in patients with younger onset than those with later onset. These results preliminarily suggest that HERV-K115 may not be associated with schizophrenia in general, but that it could play a partial role in early precipitation of the disease.

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It is also interesting to note that these polymorphic ERV's are HERV-K's, the retrovirus that has been active since our split from the chimpanzee lineage.

This doesn't explain the pattern of insertion nor the sequence comparisons that both point to common ancestry. If these insertions occurred independently then the vast majority should be non-orthologous (not at the same spot in the genome). The opposite is true. The vast majority are orthologous which is inconsistent with indepedent insertion. If these ERV's are caused by a single insertion that is then passed on through heredity then the vast majority should be orthologous, and they are. As for the sequence comparisons, your explanation does not explain why there is more LTR divergence between orthologous ERV's shared by orangutans, chimps, and humans than there is in orthologous ERV's shared by humans and chimps but not orangutaons. Common ancestry and subsequent evolution does explain these facts. The problem is that your guesses contradict the evidence we do have. So yes, you are doing worse. You are assuming that all of our ancestors possessed the same mental capacity and technological knowledge that we do. This is a very bad assumption. First of all, let's do the math. 200 lineage specific ERV's compared to 200,000 orthologous ERV's. The lineage specific ERV's only make up 0.1% of the total. 99.9% of ERV's are orthologous, or thereabouts.Secondly, you actually did describe the answer. There was an influx of ERV's into the genomes of Old World monkey and Old World great apes with the exception of humans and orangutans. You can read about it in this paper. It is a very interesting topic as to why all of these other primate species were infected by this virus but not humans nor orangutans. This retrovirus goes by the name PTERV1. From sequence analysis, it appears that this elevated influx of ERV's occurred over a relatively short time period.This also allows us to test the theory of evolution once again. Scientists found a specific retrovirus in monkeys and some great apes. The theory of evolution predicts that because it is not found in orangutans or humans, but is found in chimps and other great apes, that these insertions had to of occurred after the human and chimp lineages split. IOW, these have to be independent insertions. Therefore, these insertions will be occur at non-orthologous positions in each genome. THAT IS EXACTLY WHAT IS OBSERVED. From the paper:

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Based on an analysis of 1,467 large-insert clones, we mapped 299 retroviral insertion sites among the four species (Figure 3; Table S2). A total of 275 of the insertion sites mapped unambiguously to non-orthologous locations (Table 2), indicating that the vast majority of elements were lineage-specific (i.e., they emerged after the divergence of gorilla/chimpanzee and macaque/baboon from their common ancestor).

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Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3). We classified these as ambiguous overlap loci (Figure 3). If all 24 locations corresponded to insertions that were orthologous for each pair, this would correspond to a maximum of 12 orthologous loci. The number of non-orthologous loci was calculated as 275/287 (275 + 12) or 95.8%. This is almost certainly a lower-bound estimate owing to the limitation of our BAC-based mapping approach to refine the precise locations of the insertions. . .

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For the three intervals putatively shared between macaque and chimpanzee, we attempted to refine the precise position of the insertions by taking advantage of the available whole-genome shotgun sequences for these two genomes. For each of the three loci, we mapped the precise insertion site in the chimpanzee and then examined the corresponding site in macaque (National Center for Biotechnology Information). In one case, we were unable to refine the map interval owing to the presence of repetitive rich sequences within the interval. In two cases, we were able to refine the map location to single basepair resolution (Figures S4 and S5). Based on this analysis, we determined that the sites were not orthologous between chimpanzee and macaque. . . Although the status of the remaining overlapping sites is unknown, these data resolve four additional sites as independent insertion events and suggest that the remainder may similarly be non-orthologous.

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Precisely. Why? Studies of human DNA variation leads us to interesting conclusions. For example, the most recent common ancestor of human mitochondria existed just a few hundred thousand years ago. There were certainly other mitochondrial lineages in existence at that time, and there were after that as well. However, genetic drift lops off branches in any population, and over time only one ancient branch makes it. This is how ERV's become fixed in populations. If you looked at ERV distributions a few million years ago the picture may very well be different. Again, that does not explain the placement of these ERV's in genomes (non-orthologous vs. orthologous), nor does it explain the sequence divergence. That only applied for the ERV's that were part of that study.

Does everyone understand what I mean by "LTR divergence" and overall sequence divergence? These are very important concepts for understanding why ERV's evidence common ancestry. However, I don't want to write a long post about stuff that people already understand.

Very well. In addition to the locus (the spot at which the ERV is found), there are two other sources of phylogenetic information.The first is LTR divergence. LTR stands for long tandem repeats, and these repeat regions flank the viral genes in the middle like the two pieces of bread in a sandwich. These are often labeled 5' and 3' which relates to the beginning and end of the viral genome respectively (remember that DNA is copied in the 5' to 3' direction). When these viruses insert into the host genome the LTR's have identical or nearly identical sequence. This offers a unique source of information due to the fact that mutations will accrue in each of the LTR's after insertion into the host genome. One can determine when a mutation has occurred in one LTR by comparing it to the other LTR in the same ERV.If you want to put in some extra effort you can compare them yourself. You can find the sequence for HERV-KC4 here. You can click on the relevant LTR's and get the following links:5' LTR: link3' LTR: linkYou can then cut and paste these sequences into the LALIGN program. As you will see, they align quite well except for a few substitutions and a couple deletions/insertions. The divergence of these sequences is due to accumulated mutations since insertion. The more time that has passed since insertion the more the two LTR's will diverge. Using this information, one can estimate the time since insertion. This source of information MATCHES the time of insertion established by the locus, just as the theory of evolution predicts.The second source of phylogenetic information is the divergence of the same ERV in two different species. This one is similar to the the LTR divergence, but instead of comparing changes within the ERV itself one can compare the differences seen between orthologous ERV's in different species. The more distant the common ancestor the more divergent the orthologous ERV's will be. The phylogenies constructed from this information MATCHES (again) the phylogeny established by the locus of the ERV.Any creationist attempting to explain ERV's must explain all three sources of phylogenetic information: locus, LTR divergence, and orthologous ERV divergence between species. Any explanation that does not do all three has failed to explain ERV's.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

Why would an all powerful and all knowing supernatural deity who resides outside of space and time need to reuse designs in order to save time? For an all powerful and all knowing deity it would stand to reason that starting from scratch would take just as much effort as copying other designs.Even more, this still doesn't explain the pattern produced by locus, LTR divergence, and interspecies ERV divergence. There is no reason that a designer who reuses designs would slightly tweak DNA sequence so that it falls into a nested hierarchy through three independent analyses. When humans design things they don't produce designs that fall into a nested hierarchy, and yet this is exactly what we see in life, a nested hierarchy.The only consistent and testable explanation is common ancestry coupled with evolutionary mechanisms. Since they are trying to explain why nature is the way it is, yes. Proof is for math and alcohol. You can't prove that all of your memories before last Thursday are real memories. Keep in mind that it is possible that a devious deity could have created the universe last Thursday, complete with a false history and false memories.The fact of the matter is that we observe the only pattern of homology in life that the mechanisms of evolution can produce. All of the evidence is consistent with evolution, and there is no reason that it should be other than evolutionary mechanisms being active in the past. There is no physical law that requires chimps and humans to share orthologous ERV's. None. And yet there they are. The mechanisms of evolution have been directly observed both in the lab and in the wild. They are no more speculative than gravity or electromagnetism. The gorilla, orangutan, gibbon, and other primate genomes have not been done. As new DNA sequences are determined in primate species this group of evidence is continually testing the theory of evolution. The theory predicts that specific ERV's should be found in the genomes of these species PRIOR to their genomes being sequenced. If creationists want to truly challenge the theory of evolution here is their chance. They can start sequencing primate genomes and find sequences that do not line up with the predictions of the theory. I think we all know why creationists are not doing this, because they know deep down that the theory is correct. Why else would they pass up such an obvious chance to prove the theory false? Why do you have difficulties believing this?

If a nested hierarchy is not the pattern of homology predicted by the theory of evolution for primates then please tell us what pattern of homology the theory does predict. Please show how the mechanisms of evolution can produce anything other than a nested hierarchy with reference to ERV locus, ERV LTR divergence, and interspecies ERV sequence divergence.

So if I can find a feature that performs the same function but is designed differently then this would be inconsistent with creationism/ID?Also, why would you re-use designs so that they fall into a nested hierarchy? Staying on topic with respect to ERV's, let's say you have created chimps and orangutans, and now you have decided to make humans using a "similar mold". Why would you only use ERV's that orangutans and chimps share, but not ERV's only found in orangutans? What reason is there for this pattern of re-use? Couldn't you just as easily throw in a few hundred orangutan specific ERV's? As the old saw goes, proof is for math and alcohol. In science there is no proof. There is only evidence. Theories are never proven, they are only tested. The theory of evolution predicts what pattern of homology we should see in the placement, LTR divergence, and interspecies ERV homology for ERV's. We then look to see if this pattern is present. It is. A theory that is capable of making very accurate predictions is a good theory, wouldn't you agree? If the theory of evolution is false, why is it able to make such accurate predictions? It would seem to me that only accurate theories make accurate predictions, wouldn't you agree? How is this sleight of hand?What your argument boils down to is this. All the evidence certainly makes it look like humans and chimps share a common ancestor, and all of the evidence is consistent with evolutionary mechanisms being active in the past, but this doesn't mean that humans and chimps share a common ancestor nor does it point to evolution. That's it in a nutshell, is it not?As to species evolving into new species, this is the evidence of just that. Humans and chimps are separate ape species. The evidence clearly shows that they share a common ancestor. The DNA differences seen in the two genomes is consistent with the evolutionary mechanisms of mutation, selection, and divergence. ERV's are evidence of just what you ask for, species evolving into new species. It is the placement and sequence of ERV's that gives the theory of evolution credence. It is not ERV's themselves which add credence, it is the pattern of homology that adds credence. It is this pattern that creationists must explain, and they fail miserably every time. You have not even dealt with the pattern of homology other than to say humans were made from the same mold. This, in no way, tells us why we see a nested hierarchy. However, a nested hierarchy is EXACTLY what we should see if evolution and common ancestry is true.

What mechanisms are you basing this prediction on?What you have to remember is that the predictions pertaining to ERV's are not wild ass guesses. These predictions are based on our observations of the mechanisms of evolution in action. From these observations scientists are able to predict what we should see in genomes if these same evolutionary mechanisms were active in the past. The loci, LTR divergence, and interspecies divergence are part of those predictions. Why not? Yes, they do. The theory makes specific predictions about the features and DNA sequence of ERV's. The ERV's are then sequenced. Those predictions are found to be accurate. This is EXACTLY how one validates a theory, but testing the predictions that the theory makes. That is not what we are doing. The mere existence of predictions is not what validates the theory of evolution. It is the existence of ACCURATE AND TESTED predictions which validates the theory.Do you honestly think that because scientists claim that an ERV shared by orangutans and humans should also be found in chimps at the same spot in the genome will make an ERV magically appear in that exact position? Are you saying that making a prediction somehow makes the data appear? But that is exactly what we do see in ERV's. That is why I explained LTR divergence. The LTR's in an ERV are identical at the time of insertion. Over time mutations accumulate in each of the LTR's leading to LTR's that are no longer identical. The rate at which these mutations accumulate is consistent with neutral genetic drift in the vast majority of cases. They are perfect examples of how evolution occurs, and how speciation results in sequence divergence. That would be your difficulty, not mine. Quantum mechanics is difficult to accept when you first learn of it, but that doesn't stop Quantum mechanics from being an accurate theory. The orthologous nature of ERV's demonstrates common ancestry even if the ERV is in two individuals from the same population. You and your siblings (or cousins for that matter) share ERV's in the same spots in your genome. This is due to common ancestry.As for evolution, the [i]differences[/] in the sequence of ERV's is explained by evolutionary mechanisms, including the divergence of ERV sequences in different lineages. Evolution explains both the similarities and the differences. Read that last sentence over and over until it sinks in. It is a very important to understand how this is. Why would it be wrong when the theory is able to accurately predict the placement and sequence divergence of ERV's? That doesn't change the fact that the theory of evolution accuratley predicts the features of ERV's. You claim it isn't evolution, and yet all of the evidence is consistent with evolution. What do you think I have been talking about? The comparison of ERV's in different species is just that test. This is off topic so I will only point you in this direction. Compare the cephalopod eye to the human eye. They are designed different yet perform the same function.

Design does not imply intelligence. There are stars that produce the shape of a dipper (or plow for our British friends). However, this does not mean that someone placed the stars in the sky so that they would form the shape of a dipper (or plow).

Let's use a different analogy. Let's look at languages. The word for the number one in French, Spanish, and Italian are une, uno, and uno respectively. For Spanish and Italian the same spelling is pronounced a little bit differently. Now what are the chances that three languages independently all arrived at similar words for the same thing? Pretty low, right? Why would groups of people that do not speak each others language all come around to using very similar words? The answer is that they didn't. These languages share a common root language, Latin. These languages diverged from this common ancestor. Over time these populations were isolated and small changes accumulated in each. Over time the resulted in languages that were modified to the point that the different populations have a tough time understanding each other, but it is obvious from an analysis of the languages that they share a common root language. This is how the determination of common ancestry works, shared features that can only be explained by common ancestry plus modifications in each lineage that are not seen in the other lineages. For ERV's, these DNA sequences are obviously derived from a common source and when we compare different species we see differences in the sequence that are caused by lineage specific changes. Common ancestry is not the prediction. Common ancestry is the conclusion drawn from the evidence. In science, hypotheses are IF - THEN propositions. If A then B. If common ancestry is true then we should find a specific pattern of orthologous ERV's, LTR divergence, and ERV divergence. We then sequence the DNA and see if the hypothesis is supported, and it is. That is how science works. What ERV's do show us is:1) Divergent species share a common ancestor.
2) Lineage specific mutations accumulate over time.
3) The rates at which mutations accumulate in different genes differs due to natural selection. Mutations in ERV's tend to accumulate at a rate consistent with neutral drift. That is, mutations in ERV's tend not to affect fitness. When we compare the number of mutations in ERV's to coding regions we see more mutations in ERV's than in coding regions. This points to natural selection.For evolution to work you need divergence. That is the biggy. ERV's show that this does occur. This is exactly what ERV's show. They demonstrate descent with modification, as the poster above discusses. The ERV's descend from a common ancestor, and they are modified in each lineage through mutation and selection. The evidence for all of these mechanisms are seen in the ERV's. We have the results of that process right here and right now. For chimps and humans, by comparing their genomes you can observe the results of 5-7 million years of evolution. Our differing morphology is due to our differences in DNA. Those differences are the result of mutation and selection, as demonstrated by ERV's.

You should ask yourself why you need to be protected from the facts. Why do you see an impossibility? Why isn't this evidence? The theory of evolutions proposes that variation is produced through mutation and selection. This is exactly what we observe, variation arising through mutation and selection. When a population is split into two this causes different variations to accumulate in each population over time leading to new species which has also been observed. Again, common ancestry is the conclusion. It could very well be that there are species who do not share common ancestry. There is nothing in the theory of evolution which states that species MUST share a common ancestor. Rather, the theory of evolution tells us what evidence to look for if two species share a common ancestor. This is the prediction, the if part.In fact, scientists looking at microorganisms found in deep sea vents may find a species that does not use the same codons as the rest of life on Earth. For example, this new species may use TGA to code for methionine instead of the ATG used by the rest of life on Earth. The scientists would correctly conclude that such a species does not share common ancestry with the rest of life on Earth. There is nothing in the theory of evolution that prohibits such a conclusion.Getting back to the topic, if it was found that very few if any ERV's fell into the predicted pattern then this would spell big trouble for the conclusion of common ancestry. You are confusing the past and the future. If evolution occurred in the past then we should see specific pattern of homology, and we do. As evolution continues we will continue to see this same branching pattern, but there is no way to predict what features will evolve in each branch.As an analogy, science has a very firm grasp on the scientific explanation for rain. However, due to the chaotic and random nature of interactions in the atmosphere it is nearly impossible to predict if it will be raining a month from now. Does that this scientific explanation for rain is disqualified? Natural selection is a mechanism which, in combination with other mechanisms, does result in evolution of species. However, it does take more than just natural selection. You also need the production of new variation (mutation), and genetic isolation of populations. When all three mechanisms are in place there is nothing that will stop the production of a new species. Take a look at donkeys and horses. The fact that they are able to produce viable hybrids evidences shows that they must have shared a common ancestor in the past. However, these hybrids (mules) are sterile. There is no genetic flow between the horse and donkey population, and over time the DNA of these two populations will continue to be more and more different just as French, Italian, and Spanish became different languages from a common root language. It's a conclusion based on facts. The pattern of similarities and dissimilarities within ERV's between different species evidences the actions of natural selection, mutation, and genetic isolation--the three mechanisms that I describe above. I would hardly call something that is backed by mountains of evidence a belief.