Insertion Hot-spots destroy the ERV argument for naturalistic common-ancestry of humans and chimps

Peter Berean

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Thesis:

Insertion Hot-spots destroy the ERV argument for naturalistic common-ancestry of humans and chimps

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P1. The atheist-evolutionist ERV argument is basically a probability argument.

I.e., allegedly, there are viral segments inserted into common spots in human and chimp and ape lineages that prove common ancestry of humans and chimps. Allegedly, the probability of independent viral insertion at those common spots in these different lineages is too low to happen by random-chance. However, this atheist-argument is FALSE. See below.

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P2. Insertion Hot-spots destroy the ERV argument for naturalistic common ancestry of humans and chimps.

See below for detail.

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P3. If there are insertion HOT-SPOTS where alleged-viral-elements selectively insert, then the presence of alleged viral-elements at common spots (in different genomes) is NOT Proof of common ancestry…

… since the alleged-viral-elements could selectively insert at those hot-spots rather than randomly in the genomes. The reality is that there is LOTS of evidence for insertion hot-spots. See P3.

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P4. The presence of introns at a common locus is NOT proof of Common-Ancestry ->

Scientific-Evidence-4a:

Quote //Remarkably, we have found many cases of parallel intron gains at essentially the same sites in independent genotypes. This strongly argues against the common assumption that when two species share introns at the same site, it is always due to inheritance from a common ancestor.//

--- (Evolutionary biologist Michael Lynch. Source: Wenli Li et al, "Recent Intron Gains in Daphnia Populations", Science 27 Nov 2009: Vol. 326, Issue 5957, pp. 1260-1262).

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P5. Lots of Evidence for Insertion HOT-SPOTS

Scientific-Evidence-5a.

Quote //…a common mechanism exists for the insertion of many repetitive DNA families into new genomic sites. A modified mechanism for site-specific integration of primate repetitive DNA sequences is provided which requires insertion into dA-rich sequences in the genome. This model is consistent with the observed relationship between galago Type II subfamilies suggesting that they have arisen not by mere mutation but by independent integration events.//

--- (Ref: Gary R. Daniels, Prescott L. Deininger, "Integration site preferences of the Alu family and similar repetitive DNA sequences", Nucleic Acids Research, Volume 13, Issue 24, 20 December 1985, pp. 8939–8954)

Scientific-Evidence-5b:

Quote //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. //

--- (Source: Eugene E. Sverdlov, "Perpetually mobile footprints of ancient infections in human genome", FEBS Letters, Volume 428, Issues 1–2, 22 May 1998, pp. 1-6)

NOTE -> hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically. //

--- (Eugene E. Sverdlov, "Perpetually mobile footprints of ancient infections in human genome", FEBS Letters, Volume 428, Issues 1–2, 22 May 1998, pp. 1-6)

Scientific-Evidence-5c:

Evidence of Site-specific insertion. Quote //integrated viruses are preferentially detected in chromatin regions characterized by an open structure, a hallmark of actively transcribed genes. Target site selection might be influenced by several factors, including the function of cellular proteins that interact with integrase, the viral protein that catalyzes the integration reaction. Interestingly, a common functional feature that unifies these cellular co-factors is that, to a different extent, they are all involved in the regulation of chromatin structure or transcription.//

--- (Reference: Cereseto A, Giacca M., "Integration site selection by retroviruses", AIDS Rev. 2004 Jan-Mar;6(1):13-21.)

Scientific-Evidence-5d:

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

--- (Mitchell RS, Beitzel BF, Schroder ARW, Shinn P, Chen H, Berry CC, et al. (2004) Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences. PLoS Biol 2(8): e234. https://doi.org/10.1371/journal.pbio.0020234)

Scientific-Evidence-5e:

Quote //each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection//

Note: As we have discussed, if there are insertion HOT-SPOTS where alleged-viral-elements selectively insert, then the presence of alleged viral-elements at common spots (in different genomes) is NOT Proof of common ancestry, since the alleged-viral-elements could selectively insert at those hot-spots rather than randomly in the genomes.

Conclusion: So, the Existence of Insertion Hot-spots (as above) destroys the ERV argument for naturalistic common ancestry of humans and chimps.

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P6. Reason for Insertion Hot-Spots.

A proposal in the scientific literature for why there are insertion hot-spots: “virus-specific binding of integration complexes to chromatin features likely guides site selection.”

--- (Source: Mitchell RS, Beitzel BF, Schroder ARW, Shinn P, Chen H, Berry CC, et al. (2004) Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences. PLoS Biol 2(8): e234. https://doi.org/10.1371/journal.pbio.0020234)

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P7. ERVs violate the Nested Hierarchy that evolutionists expect from common ancestry.

Scientific-Evidence-7a.

Quote // We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely//

--- (Source: Chris T. Yohn et al., "Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans" PLoS Biol. 2005 Apr; 3(4): e110.).

Scientific-Evidence-7b.

Quote //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.//

--- (Source: Chris T. Yohn et al., "Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans" PLoS Biol. 2005 Apr; 3(4): e110.).

So, ERVs violate the Nested Hierarchy that evolutionists expect from common ancestry.

Conclusion: This means that the ERV argument is FALSE.

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P8. Some alleged ERVs have critical functions in the organism.

This indicates that those alleged ERV segments are critical parts of the organism's genome, and not just random viral insertions. Such functionality would appear to be evidence AGAINST the claim that these are actual viral inserted segments.

So, this would be evidence against the atheist ERV argument.

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P9. The ERV probability argument is a FAILURE.

Atheists offer about SEVEN alleged-viral elements that are in the same location in Human vs Chimp genomes, as evidence for their argument that ERVs prove naturalistic common ancestry of humans and chimps.

However, there are literally tens of thousands (let's say 20,000) alleged inserted viral-elements in the human genome and the chimp genome.

So, if 7 out of 20,000 alleged viral elements are common in location (between human and chimp genomes), that is 7/20,000 * 100 = 0.035 percent that is common.

If ONLY 0.035 percent of the evidence supports the atheist ERV argument, that is hardly a compelling argument!

So, the ERV probability argument is a FAILURE, based on the math.

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P10. There are ERVs that violate the claim of chimp-human closeness of common ancestry (over gorilla-chimp closeness).

Quote -> //We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus.//

--- Ref: Barbulescu M et al., "A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans", Curr Biol. 2001 May 15;11(10):779-83.

Comment: If ERVs are proof of common ancestry, then we would expect that this ERV should be present in chimps AND humans, and NOT in gorillas (of they arose in the alleged chimp-human LUCA ancestor). Or if the ERV came into the gorilla-chimp-human LUCA ancestor, then the ERV should be present in ALL three, chimp, human and gorilla. However, there is NO alleged human common-ancestry where there would be a chimp-gorilla common ancestor that is NOT also a common ancestor of humans.

So, if ERVs are proof of common ancestry, then the chimp-gorilla common ERV is proof of chimp-gorilla common ancestry and its ABSENCE in the human genome is proof that humans DO NOT share common ancestry with chimps later than gorillas.

However, this contradicts the atheist view that chimps and humans share a common ancestor after the gorilla-chimp split.

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P11. So, the atheist ERV argument is a failure for a variety of reasons as discussed above.

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CONCLUSIONS:

P1. Insertion Hot-spots destroy the ERV argument for naturalistic common ancestry of humans and chimps. So the atheist ERV-argument is a FAILURE.

P2. ERVs violate the Nested Hierarchy that evolutionists expect from common ancestry.
So the atheist ERV-argument is a FAILURE.

P3. The atheist-evolutionist ERV argument is basically a probability argument. But only 0.035% of the evidence is consistent with this argument. The rest CONTRADICTS the atheist argument. So the atheist ERV-probability argument is a FAILURE.

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Ref: Thanks to https://evolutionnews.org/2011/05/do_shared_ervs_support_common_/

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