ERVs Independent and identical integration sites

[lifepsyop]

This thread is to call into question the evolutionists' claim that shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent. I have spent the past few days searching the literature for studies which appear to contradict this claim and have found many results. In some studies the researchers themselves are drawing the conclusion that shared ERV integration sites should not be automatically assumed to reflect common descent, but instead may be homoplasies, or "convergent retroposon integrations".

An interesting note from the literature to start off:

SINEs of the perfect character
Hillis 1999

What of the claim that the SINE-LINE insertion events are perfect markers of evolution (i.e., they exhibit no homoplasy)? Similar claims have been made for other kinds of data in the past, and in every case examples have been found to refute the claim. For instance, DNA–DNA hybridization data were once purported to be immune from convergence, but many sources of convergence have been discovered for this technique. Structural rearrangements of genomes were thought to be such complex events that convergence was highly unlikely, but now several examples of convergence in genome rearrangements have been discovered. Even simple insertions and deletions within coding regions have been considered to be unlikely to be homoplastic, but numerous examples of convergence and parallelism of these events are now known. Although individual nucleotides and amino acids are widely acknowledged to exhibit homoplasy, some authors have suggested that widespread simultaneous convergence in many nucleotides is virtually impossible. Nonetheless, examples of such convergence have been demonstrated in experimental evolution studies.

http://www.pnas.org/content/96/18/9979.full.pdf+html

Two independent retrotransposon insertions at the same site within the coding region of BTK.
Conley et al. 2005

Insertion of endogenous retrotransposon sequences accounts for approximately 0.2% of disease causing mutations. These insertions are mediated by the reverse transcriptase and endonuclease activity of long interspersed nucleotide (LINE-1) elements. The factors that control the target site selection in insertional mutagenesis are not well understood. In our analysis of 199 unrelated families with proven mutations in BTK, the gene responsible for X-linked agammaglobulinemia, we identified two families with retrotransposon insertions at exactly the same nucleotide within the coding region of BTK.... The occurrence of two retrotransposon sequences at exactly the same site suggests that this site is vulnerable to insertional mutagenesis. A better understanding of the factors that make this site vulnerable will shed light on the mechanisms of LINE-1 mediated insertional mutagenesis.

http://www.ncbi.nlm.nih.gov/pubmed/15712380/

An ancient retrovirus-like element contains hot spots for SINE insertion.
Cantrell et al. 2001

Vertebrate retrotransposons have been used extensively for phylogenetic analyses and studies of molecular evolution. Information can be obtained from specific inserts either by comparing sequence differences that have accumulated over time in orthologous copies of that insert or by determining the presence or absence of that specific element at a particular site. The presence of specific copies has been deemed to be an essentially homoplasy-free phylogenetic character because the probability of multiple independent insertions into any one site has been believed to be nil. Mys elements are a type of LTR-containing retrotransposon present in Sigmodontine rodents. In this study we have shown that one particular insert, mys-9, is an extremely old insert present in multiple species of the genus Peromyscus. We have found that different copies of this insert show a surprising range of sizes, due primarily to a continuing series of SINE (short interspersed element) insertions into this locus. We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.

http://www.ncbi.nlm.nih.gov/pubmed/11404340

Are Transposable Element Insertions Homoplasy Free?: An Examination Using the Avian Tree of Life
Han et al. 2011

The argument that TE insertions exhibit little or no homoplasy is ultimately based upon assumptions about their biology....

The observation that independent TE insertions can occur at the exact same site in the same or different taxa, or can be precisely deleted, suggests that care needs to be taken in assigning character states for phylogenetic analyses....

Our results also suggest that TEs should not be viewed as perfect characters exempt from homoplasy. Instead, TE insertions present many of the same challenges for phylogenetic analyses as other types of data, such as nucleotide sequences.

http://sysbio.oxfordjournals.org/content/60/3/375.full.pdf+html

Evolutionary implications of multiple SINE insertions in an intronic region from diverse mammals. Yu L. et al. 2005

Particularly interesting is the finding that all identified lineage-specific SINE elements show a strong tendency to insert within or in very close proximity to the preexisting MIRs(Mammalian-wide interspersed repeats) for their efficient integrations, suggesting that the MIR element is a hot spot for successive insertions of other SINEs. The unexpected MIR excision as a result of a random deletion in the rat intron locus and the non-random site targeting detected by this study indicate that SINEs actually have a greater insertional flexibility and regional specificity than had previously been recognized. Implications for SINE sequence evolution upon and following integration, as well as the fascinating interactions between retroposons and the host genomes are discussed.

http://www.ncbi.nlm.nih.gov/pubmed/16245022

New insights into the evolution of intronic sequences of the beta-fibrinogen gene and their application in reconstructing mustelid phylogeny. Yu L. et al. 2008

....Detailed characterizations of the two intronic regions not only reveal the remarkable occurrences of short interspersed element (SINE) insertion events, providing a new example supporting the attractive hypothesis that attrition of an earlier retroposition may offer a proper environment for successive retropositions by forming a "dimer-like" structure, but also demonstrate their utility in the resolution of mustelid phylogeny.

http://www.ncbi.nlm.nih.gov/pubmed/18624576

Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements
Levy et al. 2009

Throughout evolution, eukaryotic genomes have been invaded by transposable elements (TEs). Little is known about the factors leading to genomic proliferation of TEs, their preferred integration sites and the molecular mechanisms underlying their insertion. We analyzed hundreds of thousands nested TEs in the human genome, i.e. insertions of TEs into existing ones. We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE. In particular, retrotransposed Alu elements contain a non-canonical single nucleotide hotspot for insertion of other Alu sequences. We next devised a method for identification of integration sequence motifs of inserted TEs that are conserved within the targeted TEs. This method revealed novel sequences motifs characterizing insertions of various important TE families: Alu, hAT, ERV1 and MaLR. Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition.

http://nar.oxfordjournals.org/content/38/5/1515.short

Patterns of Diversity Among SINE Elements Isolated from Three Y-Chromosome Genes in Carnivores
Slattery et al. 2000

...In contrast, sporadic insertions unrelated to species divergence, as well as clear evidence of homoplasy, are represented by Smcy in Felidae. Only one species from the domestic cat lineage, F. silvestris, possessed a SINE within Smcy, an indication that this event was unique and occurred after the Zfy insertion. The presence of this SINE within the same location with identical flanking sequences (fig. 1B)of Smcy in L. rufus, a species only distantly related to the domestic cat lineage, is likely an example of insertion dictated by the target sequences within the flanks. This provides strong evidence that SINE insertion at identical sites within different species can occur independently of phylogeny, and it counters the hypothesis that SINEs are exempt from parallel or convergent evolution.[/color]


http://mbe.oxfordjournals.org/content/17/5/825.full.pdf

I am left wondering why this type of data seems to have been consistently avoided over the years as Evolutionists (presumably a few experts on ERVs) have presented their case to the public and claimed over and over again that the chances of those ERV's sharing the same locations independent of common descent is practically impossible.

And another note on what I believe is the inherently unfalsifiable nature of the theory of Evolution:

In light of this data, it is not at all hard to imagine the "evolutionary rescue device" arising if it so happened that we discovered ERV integrations were wildly incongruent with regards to popularly phylogeny. The explanation would be that there is an as-of-yet not fully resolved biological mechanism that is attracting identical retroposon integration events. It would simply be assumed that ERV's have a tendency to reflect homoplasy. In this alternate case, the **discordant data would actually become evidence** for this hypothesis, based on prior commitments to Evolution / Common Descent being true.

 

[australopithecus]

Seems Gilbo has sent a friend. Can you let us know at what point he'll grow a spine and return to answer his critics?

 

[he_who_is_nobody]

This thread is to call into question the evolutionists' claim that shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent. I have spent the past few days searching the literature for studies which appear to contradict this claim and have found many results. In some studies the researchers themselves are drawing the conclusion that shared ERV integration sites should not be automatically assumed to reflect common descent, but instead may be homoplasies, or "convergent retroposon integrations".

I have never heard an evolutionist claim “… shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent.” It may be the most likely way, but not the only way.

[/thread]

 

[lifepsyop]

This thread is to call into question the evolutionists' claim that shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent. I have spent the past few days searching the literature for studies which appear to contradict this claim and have found many results. In some studies the researchers themselves are drawing the conclusion that shared ERV integration sites should not be automatically assumed to reflect common descent, but instead may be homoplasies, or "convergent retroposon integrations".

I have never heard an evolutionist claim “… shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent.” It may be the most likely way, but not the only way.

[/thread]

That's a funny response, considering the entire Evo argument from ERV's is directly based on that inference.

Are you then conceding that shared ERV integration sites in general should not be assumed to be a product of common ancestry?

I accept your opinion that it "may be most likely", but I am addressing those who claim ERV's as some sort of knock-down hard evidence for Common Descent.

 

[Master_Ghost_Knight]

I have always said that the ability to comprehend noise is the biggest culprit for drawing wrong conclusions from data. This also applies here.

That's a funny response, considering the entire Evo argument from ERV's is directly based on that inference.

Are you then conceding that shared ERV integration sites in general should not be assumed to be a product of common ancestry?

I accept your opinion that it "may be most likely", but I am addressing those who claim ERV's as some sort of knock-down hard evidence for Common Descent.

No. It is important here to make a distinction between the simplified models we use to explain certain concepts to layman, and what actually happens.
On the general layman explanation a unspecified ERV sequence which is inserted in one individual in a location at random which is then transmitted to subsequent generations ending out dominating the entire species and subsequently inherited by all the child species. Due to the random nature of this insertion, and statistical improbability, it can then be hypothesized that if a similar insertion is to found on 2 distinct species of unknown relation, that it is more likely that this 2 species must have shared a more closely related ascendancy than to have them pop up independently.
Right? No. Well, in general this is the case, put it is not precisely the case, and thus this crude over-simplification can be betrayed by real world counter-examples.
We can not forget that we are talking about real world examples, about process that have no particular goals or strictly defined outcomes.
If a viral genetic material is prevalent in a geographic area, it is not unlikely that multiple species would come into contact with the same material and assimilate it into their own genetic code, nor is it even unlikely for different individuals of the same species to assimilate it in different insertion points of their genome. It is also not true that any insertion point shares a equal likelihood, for once let's not forget that DNA serves the function of being transcripted into proteins that regulate the development of the organism, if the production of those proteins are disrupted by the insertion of this viral material then this can be particular detrimental to the organism which can cause it to go sterile or make it disadvantageous to its own survival, and thus removing itself from the gene pool. This will have the affect of concentrating the ERV insertion around more permissible sites. To skew this even further, the probability of certain insertions areas being affected is also related to the geometry of the genome, and thus by changing the way the DNA folds, it can change the probability density to be more favorable in some insertion points rather than others. ERV insertion points are also not immune to genetic mutation such as deletion, the downside of which is that certain more distant related species can share some ERV insertions that are not shared by more closely related species.
But does this mean that this method is unreliable to trace a phylogenetic tree? No. And even the papers that you yourself linked (but not read) say that much. What they show is that you shouldn't jump to conclusions out of very restricted data (as you just did) because they can be decieving, and you should instead use more extensive and statistically significant data sets if you want to draw conclusions.
In the real world, things are not so simple, and there are allot of complications that makes not straight forward (if anything appears straight forward in science, it is because you have not learned enough), but this doesn't mean that the science is all wrong or that scientists don't know what they are doing. Quite the contrary, the fact that they found all this complications (that would just go over the head for most of the people) and corrected for it means that they are doing a good job.

 

[he_who_is_nobody]

That's a funny response, considering the entire Evo argument from ERV's is directly based on that inference.

No, it is not.

Are you then conceding that shared ERV integration sites in general should not be assumed to be a product of common ancestry?

You are confusing two different things here. There is such a thing as an independent ERV insertion (i.e. a virus inserts itself across multiple lineages in a short matter of time). There are also ERVs that can be traced through common ancestry (a virus inserted itself in a single lineage several generations ago). One has to remember that ERVs are used as another confirmation of common descent.

I accept your opinion that it "may be most likely", but I am addressing those who claim ERV's as some sort of knock-down hard evidence for Common Descent.

The knockdown argument for common descent is genetics, QED.

 

[lifepsyop]

I have always said that the ability to comprehend noise is the biggest culprit for drawing wrong conclusions from data. This also applies here.

That's a funny response, considering the entire Evo argument from ERV's is directly based on that inference.

Are you then conceding that shared ERV integration sites in general should not be assumed to be a product of common ancestry?

I accept your opinion that it "may be most likely", but I am addressing those who claim ERV's as some sort of knock-down hard evidence for Common Descent.

No. It is important here to make a distinction between the simplified models we use to explain certain concepts to layman, and what actually happens.
On the general layman explanation a unspecified ERV sequence which is inserted in one individual in a location at random which is then transmitted to subsequent generations ending out dominating the entire species and subsequently inherited by all the child species. Due to the random nature of this insertion, and statistical improbability, it can then be hypothesized that if a similar insertion is to found on 2 distinct species of unknown relation, that it is more likely that this 2 species must have shared a more closely related ascendancy than to have them pop up independently.
Right? No. Well, in general this is the case, put it is not precisely the case, and thus this crude over-simplification can be betrayed by real world counter-examples.

That's the problem, you don't know if that is generally the case. You just baldly asserted it. It is assumed. And it does not fit evolutionary predictions, as I've posted here http://www.leagueofreason.org.uk/viewtopic.php?f=8&t=11867 ERV's contradict the entire placental mammalian tree.

We can not forget that we are talking about real world examples, about process that have no particular goals or strictly defined outcomes.
If a viral genetic material is prevalent in a geographic area, it is not unlikely that multiple species would come into contact with the same material and assimilate it into their own genetic code, nor is it even unlikely for different individuals of the same species to assimilate it in different insertion points of their genome. It is also not true that any insertion point shares a equal likelihood, for once let's not forget that DNA serves the function of being transcripted into proteins that regulate the development of the organism, if the production of those proteins are disrupted by the insertion of this viral material then this can be particular detrimental to the organism which can cause it to go sterile or make it disadvantageous to its own survival, and thus removing itself from the gene pool. This will have the affect of concentrating the ERV insertion around more permissible sites. To skew this even further, the probability of certain insertions areas being affected is also related to the geometry of the genome, and thus by changing the way the DNA folds, it can change the probability density to be more favorable in some insertion points rather than others. ERV insertion points are also not immune to genetic mutation such as deletion, the downside of which is that certain more distant related species can share some ERV insertions that are not shared by more closely related species.

Good information. Now you can also add that ERV's are reported to insert at identical loci in unrelated genomes, with inference to an integration mechanism that may be inducing it.

Now tell me how you know, or what experiment you've conducted that tells you any number of the ERV's that you consider evidence of common descent, aren't actually independently acquired?

But does this mean that this method is unreliable to trace a phylogenetic tree? No.

What makes it empirically reliable?

And even the papers that you yourself linked (but not read) say that much. What they show is that you shouldn't jump to conclusions out of very restricted data (as you just did) because they can be decieving, and you should instead use more extensive and statistically significant data sets if you want to draw conclusions.

How am I jumping to conclusions by 1) showing evidence of ERV homoplasies 2) asking for evidence that other ERVs aren't homoplasies. ? For years now, who has been jumping to conclusions about ERVs? Evolutionists. You are the ones making the claims, based on assumptions about the nature of ERV integrations, and demanding the world accept them as scientific. What has been the central claim forcefully preached in evo debate forums across the internet? "The chances of ERVs being located in the same spot across X animal groups without being inherited is impossible!"

In the real world, things are not so simple, and there are allot of complications that makes not straight forward (if anything appears straight forward in science, it is because you have not learned enough), but this doesn't mean that the science is all wrong or that scientists don't know what they are doing. Quite the contrary, the fact that they found all this complications (that would just go over the head for most of the people) and corrected for it means that they are doing a good job.

Is this supposed to be in response to an argument I made? I never suggested "all science is wrong" or anything to that effect.

 

[Rumraket]

This thread is to call into question the evolutionists' claim that shared Endogenous Retrovirus integration sites should not be inferred to be shared by any other means than by inheritance via common descent.

Which would be pretty meaningless, since that fact has been known for almost 2 decades now. In other words, you're not telling us something evolutionary biologists don't already know and haven't worked out how to control for.

I have spent the past few days searching the literature for studies which appear to contradict this claim and have found many results.

Good for you, did you also happen to speciously elect to filter out the parts of the many different papers you cite which explain how to control for homoplasy vs common descent? No? That's.... strange.

In some studies the researchers themselves are drawing the conclusion that shared ERV integration sites should not be automatically assumed to reflect common descent, but instead may be homoplasies, or "convergent retroposon integrations".

Correct, and the difference can be inferred by doing sequence alignments of the specific LINE's/SINE's.

For example, if a LINE/SINE is shared through common descent over multiple speciation events, sequence alignments can be used to construct phylogenetic trees that confirm the phylogeny because the sequences will be evolving at a neutral rate.

An interesting note from the literature to start off:

SINEs of the perfect character
Hillis 1999

What of the claim that the SINE-LINE insertion events are perfect markers of evolution (i.e., they exhibit no homoplasy)? Similar claims have been made for other kinds of data in the past, and in every case examples have been found to refute the claim. For instance, DNA–DNA hybridization data were once purported to be immune from convergence, but many sources of convergence have been discovered for this technique. Structural rearrangements of genomes were thought to be such complex events that convergence was highly unlikely, but now several examples of convergence in genome rearrangements have been discovered. Even simple insertions and deletions within coding regions have been considered to be unlikely to be homoplastic, but numerous examples of convergence and parallelism of these events are now known. Although individual nucleotides and amino acids are widely acknowledged to exhibit homoplasy, some authors have suggested that widespread simultaneous convergence in many nucleotides is virtually impossible. Nonetheless, examples of such convergence have been demonstrated in experimental evolution studies.

http://www.pnas.org/content/96/18/9979.full.pdf+html

This very same paper also goes on to explain how the to tell the difference between homoplasy and common descent, besides also establishing that the level of homoplasy is comparatively low.

In other words, homoplasy does not constitute the obstacle you're trying to pretend it is, and evolutionary biologists know how to control for it. The same basically goes for all the rest of the papers you link. Homoplasy can be detected through standard phylogenetic methods and distinguished from common descent.

I am left wondering why this type of data seems to have been consistently avoided over the years as Evolutionists (presumably a few experts on ERVs) have presented their case to the public and claimed over and over again that the chances of those ERV's sharing the same locations independent of common descent is practically impossible.

It hasn't. Quite simply. You seem to be laboring under the misapprehension that the mere detection of an ERV in the same approsimate location in two independent genomes is taken as evidence of common descent. It is not, they still have to do sequence alignments from multiple species to discriminate between homoplasies and actual decent.

It would also seem strange to claim that evolutionary biologists are somehow shielding this information from the public when it's right there, publicly available. Perhaps the issue is significantly less nefarious than you seem wanting to insinuate, and instead of boring the public with a lot of technical detail surrounding the different possible phylognetic methods (how to do alignments, construct trees, root them with outgroups, control for homoplasies, long branch attractions etc. etc. - biologists have elected instead of just explain a small set of basic facts to give at least a basic understanding of what is going on.

If the public then wants to explore the subject further, they can go and educate themselves and buy actual textbooks and takes courses in computational molecular evolution and molecular phylogenetics.

And another note on what I believe is the inherently unfalsifiable nature of the theory of Evolution:

In light of this data, it is not at all hard to imagine the "evolutionary rescue device" arising if it so happened that we discovered ERV integrations were wildly incongruent with regards to popularly phylogeny. The explanation would be that there is an as-of-yet not fully resolved biological mechanism that is attracting identical retroposon integration events.

You can make shit up all day long, it's not going to make it a fact. This is simply an exposition into your personal paranoia about a scientific field you're psychoemotionally predisposed to dismiss out of hand before having properly educated yourself enough to fully understand.

It would simply be assumed that ERV's have a tendency to reflect homoplasy. In this alternate case, the **discordant data would actually become evidence** for this hypothesis, based on prior commitments to Evolution / Common Descent being true.

No. The problem is that you don't seem to understand that the evidence for evolution from molecular phylogenetics is statistical in nature. That means there's a pattern supported by a significant statistical weight that implies common descent. This pattern could technically easily be falsified, you would simply have to show that, on average, the number of sites divergent from the "main pattern" expected if common descent was true, were outweighing the number of sites congruent with common descent.

Such tests have been done on some of the most difficult organisms to infer phylogenies from (fast-evolving single-celled organisms prone to horizontal gene transfer), using large clusters of genes and producing multiple aligments.
See for example tests such as this:
http://www.biomedcentral.com/1741-7007/11/46
Seeing the Tree of Life behind the phylogenetic forest
Pere Puigbò, Yuri I Wolf and Eugene V Koonin*

We set out to address the above question as objectively as possible, first of all dispensing with any pre-selected standard of tree-like evolution. The analyzed FOL consisted of 6,901 maximum likelihood phylogenetic trees that were built for clusters of orthologous genes from a representative set of 100 diverse bacterial and archaeal genomes [1]. The complete matrix of topological distances between these trees was analyzed using the Inconsistency Score, a measure that we defined specifically for this purpose that reflects the average topological (in)consistency of a given tree with the rest of the trees in the FOL (for the details of the methods employed in this analysis, see [21]). Although the FOL includes very few trees with exactly identical topologies, we found that the topologies of the trees were far more congruent than expected by chance. The 102 Nearly Universal Trees (NUTs; that is, the trees for genes that are represented in all or nearly all archaea and bacteria), which include primarily genes for key protein components of the translation and transcription systems, showed particularly high topological similarity to the other trees in the FOL. Although the topologies of the NUTs are not identical, apparently reflecting multiple HGT events, these transfers appeared to be distributed randomly. In other words, there seem to be no prominent ‘highways’ of HGT that would preferentially connect particular groups of archaea and bacteria. Thus, although the NUTs cannot represent the FOL completely, they appear to reflect a significant central trend, an attractor in the tree space that could be equated with the STOL (Figure 1)

.
The central tree-like trend in the phylogenetic forest of life. The circles show genomes of extant species and the grey tree in the background shows the statistical central trend in the data. For the purpose of illustration, the figure shows an 'FOL' made of 16 trees with 20 deviations from the central tree-like pattern.
Puigbò et al. BMC Biology 2013 11:46 doi:10.1186/1741-7007-11-46

So even where you would have the most reason to think inferring an actual phylogenetic tree was the least likely, because of both HGT events and the extremely fast evolving nature of single-celled organisms, a significant statistical trend was still detected that implied an actual tree of life.

(There are many studies like this one that all conclude basically the same thing). This underscores what tried to explain above, there is a singificant statistical weight in favor of tree-like descent, even when all the confounding factors are included. The number of sites congruent with the nested hierachy expected from common descent STILL significantly outweighs the number of divergent sites. The most plausible and simples explanation for this observation is common descent. This could have been different, the trees could have disagreed more than they could have converged, and they could have disagreed to an extremely high statistical degree. But they DON'T, they do the opposite. Common descent is therefore still massively statistically attested.

This very same fact is true for ERV's, the number of sites shared due to common descent significantly outweighs the number of sites shared due to homoplasies.
See for example:
http://www.evolutionarymodel.com/ervs.htm

d) The fourth common response is to understate the number of ERVs in identical loci, and to use that number in conjunction with target site preference. The argument is as follows:

There are only a few ERVs found in identical loci in both humans and chimpanzees. Given target site preference, it is not unlikely that they are the result of infections in separate lineages. Thus the sharing of ERVs is constant with uncommon ancestry.

It is not unreasonable to hypothesize that among the tens of thousands of ERVs, similar target site preference may have resulted in a very small percentage of instances of insertion, endogenization, and fixation in identical loci in two separate lineages.

But the first problem with the idea that this renders uncommon ancestry plausible is that there are ERVs shared by many more than just two lineages. For instance, there are ERVs shared by chimpanzees, humans, gorillas, orangutans, gibbons, and Old World Monkeys (Kurdyukov et al., 2001; Lebedev et al., 2000). The second problem—and by far, the most important—is that we do not share only a few ERVs in identical loci with Chimpanzees; examination of indel variation, and whole-genome analysis shows that we share virtually all of them with Chimpanzees. This is discussed extensively in the "Amount of Shared ERVs" section, above.

Conclusion

Ultimately, the best way to respond to such claims—after having addressed their points specifically, of course—is to relentlessly drive home what they seem least willing to discuss; that deviation from patterns is to be expected, and that the corroboratory patterns of distribution, mutation, and LTR-LTR discontinuity are solely explicable by the evolutionary model.

Since these ERV's are also mostly junk, they are evolving at a neutral rate, accumulating mutations over time. As speciation events happen further and further back in time, even single ERV sites shared between multiple species accumulate mutations such that the pattern you get when doing sequence alignments from their sites still produce a nested hierarchy congruent with common descent.

 

[Rumraket]

Now tell me how you know, or what experiment you've conducted that tells you any number of the ERV's that you consider evidence of common descent, aren't actually independently acquired?

Sequence alignments from multiple species. If the LINEs/SINEs are shared through common descent, they will be accumulating mutations at a neutral rate, and sequence alignments can be used to construct phylogenetic trees, just like with any other orthologues gene(or genomic loci) shared by multiple species.

It's that simple.

 

[Rumraket]

I accept your opinion that it "may be most likely", but I am addressing those who claim ERV's as some sort of knock-down hard evidence for Common Descent.

No single ERV SINE or LINE insertion can be taken as a knock-down argument for common descent. It is the fact that there are thousands of them and that they massively statistically outweigh the discordant ones to an extremely high degree.

If you want to be really rigorous, you can do whole genome analysis and produce your alignments using the full set of orthologous pairs shared between all species for which you want to test whether ancestry can be inferred. Though it should be said, doing whole-genome(or at least, phylogenies using all orthologoues pairs) phylogenies for multiple species is extremely computationally demanding. That's why biologists usually just select a core set of genes (big enough to be statistically significant and represent an average picture of the genome of the organism, through small enough to be handleable by extant computer hardware).

Many such phylogenies have been done, see for example:
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0069924

Beyond Reasonable Doubt: Evolution from DNA Sequences
W. Timothy J. White equal contributor, Bojian Zhong equal contributor, David Penny mail

Abstract

We demonstrate quantitatively that, as predicted by evolutionary theory, sequences of homologous proteins from different species converge as we go further and further back in time. The converse, a non-evolutionary model can be expressed as probabilities, and the test works for chloroplast, nuclear and mitochondrial sequences, as well as for sequences that diverged at different time depths. Even on our conservative test, the probability that chance could produce the observed levels of ancestral convergence for just one of the eight datasets of 51 proteins is ≈1×10[sup]−19[/sup] and combined over 8 datasets is ≈1×10[sup]−132[/sup]. By comparison, there are about 10[sup]80[/sup] protons in the universe, hence the probability that the sequences could have been produced by a process involving unrelated ancestral sequences is about 10[sup]50[/sup] lower than picking, among all protons, the same proton at random twice in a row. A non-evolutionary control model shows no convergence, and only a small number of parameters are required to account for the observations. It is time that that researchers insisted that doubters put up testable alternatives to evolution.

A dataset of 51 protein sequences is a pretty large set of data to use to infer phylogenies with. If common descent was false, there'd be no expectation that all these different proteins would so massively statistically attest to the same basic phylogeny.

This is pretty much game over for anything other than evolution by common descent.

 

[Rumraket]

What has been the central claim forcefully preached in evo debate forums across the internet? "The chances of ERVs being located in the same spot across X animal groups without being inherited is impossible!"

No it has not. Or at least, more correctly, If anyone has been advancing such an argument, they were wrong. I have already explained how ERV insertions support common ancestry above. The nature of that argument is not what you portray here.

 

[lifepsyop]

For example, if a LINE/SINE is shared through common descent over multiple speciation events, sequence alignments can be used to construct phylogenetic trees that confirm the phylogeny because the sequences will be evolving at a neutral rate.

References please.

Is this pattern ever violated and explained as a sequence becoming conserved by selection?

In other words, homoplasy does not constitute the obstacle you're trying to pretend it is, and evolutionary biologists know how to control for it. The same basically goes for all the rest of the papers you link. Homoplasy can be detected through standard phylogenetic methods and distinguished from common descent.

Of course they know how to "control for it". In standard phylogeny, a homoplastic trait can become a homologous one and vice versa, if it is shown to help "resolve" a most "parsimonious" tree. Homoplasy is not detected in any objective sense of the word. It is statistically inferred, and can be arbitrarily reversed if it results in greater phylogenetic "resolution".

And another note on what I believe is the inherently unfalsifiable nature of the theory of Evolution:

In light of this data, it is not at all hard to imagine the "evolutionary rescue device" arising if it so happened that we discovered ERV integrations were wildly incongruent with regards to popularly phylogeny. The explanation would be that there is an as-of-yet not fully resolved biological mechanism that is attracting identical retroposon integration events.

You can make shit up all day long, it's not going to make it a fact. This is simply an exposition into your personal paranoia about a scientific field you're psychoemotionally predisposed to dismiss out of hand before having properly educated yourself enough to fully understand.

I'm not making it up. That's how evolutionists actually think. Whenever something appears problematic for Evolution, even "astonishingly" unexpected from an evolutionary perspective, in the very next breath it is automatically absorbed as new evidence for how Evolution works. The literature is full of such examples.

The problem is that you don't seem to understand that the evidence for evolution from molecular phylogenetics is statistical in nature. That means there's a pattern supported by a significant statistical weight that implies common descent. This pattern could technically easily be falsified, you would simply have to show that, on average, the number of sites divergent from the "main pattern" expected if common descent was true, were outweighing the number of sites congruent with common descent.

Give me a hypothetical example with specific animal groups. Don't just show me a picture of a spaghetti diagram and baldly assert that we should get those results if common descent is false.

Such tests have been done on some of the most difficult organisms to infer phylogenies from (fast-evolving single-celled organisms prone to horizontal gene transfer), using large clusters of genes and producing multiple aligments.
See for example tests such as this:
http://www.biomedcentral.com/1741-7007/11/46
Seeing the Tree of Life behind the phylogenetic forest
Pere Puigbò, Yuri I Wolf and Eugene V Koonin*
Although the FOL includes very few trees with exactly identical topologies, we found that the topologies of the trees were far more congruent than expected by chance.

.

More congruent than expected by chance? What exactly does this mean? If genomes were randomly assembled all at once?

(There are many studies like this one that all conclude basically the same thing). This underscores what tried to explain above, there is a singificant statistical weight in favor of tree-like descent, even when all the confounding factors are included. The number of sites congruent with the nested hierachy expected from common descent STILL significantly outweighs the number of divergent sites. The most plausible and simples explanation for this observation is common descent. This could have been different, the trees could have disagreed more than they could have converged, and they could have disagreed to an extremely high statistical degree. But they DON'T, they do the opposite. Common descent is therefore still massively statistically attested.

There is a deep flaw in this reasoning, and that is the metaphysical assumption that only common descent can explain nested hierarchies. Without explanation, you demand that trees should be a chaotic mess if Common Descent is false. Why? What's your reasoning?

Do you believe we should observe wildly discordant things like Dogs grouping with Termites and Whales grouping with Pine Cones if common descent is false?

This very same fact is true for ERV's, the number of sites shared due to common descent significantly outweighs the number of sites shared due to homoplasies.

What is your objective criteria for distinguishing homology vs. homoplasy?

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

.....But the first problem with the idea that this renders uncommon ancestry plausible is that there are ERVs shared by many more than just two lineages. For instance, there are ERVs shared by chimpanzees, humans, gorillas, orangutans, gibbons, and Old World Monkeys (Kurdyukov et al., 2001; Lebedev et al., 2000). The second problem—and by far, the most important—is that we do not share only a few ERVs in identical loci with Chimpanzees; examination of indel variation, and whole-genome analysis shows that we share virtually all of them with Chimpanzees. This is discussed extensively in the "Amount of Shared ERVs" section, above.

This is a strawman as I never made the argument that the pattern of shared ERV insertions could be explained by the odds, or by chance. (I believe this is known as the Birthday Paradox)

My argument is that there is evidence of highly insertion-site-specific integration mechanisms. And many researchers have admitted they know very little about how the integration process actually works. There is a progressive pattern of discovering less and less randomness to the process then was previously assumed, even down to identical nucleotide insertions.

Evolutionists are assuming the integration sites could not be that specific. If it happens, it is rare. How do you know it is rare?

Since these ERV's are also mostly junk, they are evolving at a neutral rate, accumulating mutations over time. As speciation events happen further and further back in time, even single ERV sites shared between multiple species accumulate mutations such that the pattern you get when doing sequence alignments from their sites still produce a nested hierarchy congruent with common descent.

References please.

And if by contrast, sequences do not appear to be "evolving" at a neutral rate, why can't the evolutionist simply infer that they must have contributed to fitness and conserved by selection? They could be highly conserved in one specific lineage, and neutral in another, in order to explain any pattern of rate of change in sequence alignment.

 

[Rumraket]

For example, if a LINE/SINE is shared through common descent over multiple speciation events, sequence alignments can be used to construct phylogenetic trees that confirm the phylogeny because the sequences will be evolving at a neutral rate.

References please.

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

Layer 2
As previously explained, although the LTRs of a provirus must be identical upon insertion, once endogenized, they begin accumulating mutations. Any mutations to one LTR become quite apparent, as they are not accompanied by the same mutations in the other. Thus each mutation causes the ratio of discontinuity between the two LTRs of a full-length ERV to increase. Since ERVs in identical loci among greater numbers species of wider taxonomic separation correlate to older insertions, if the evolutionary model is correct, they should also have higher ratios of discontinuity between their LTRs. And what do we find? We find just that; a pattern, where the degree of a shared ERVs’ LTR-LTR discontinuity is proportional to the degree of taxonomic separation between the species that share it (Johnson and Coffin, 1999). There is deviation from the pattern—likely caused by viral transfer and interelement recombination/conversion (Hughes & Coffin, 2005) and viral transfer (Belshaw et al., 2004)—but the pattern is holds for many full-length ERVs and is explainable only by decent with modification from a specific series of common ancestral species. Once again, we see strong evidence for ERV orthology.

Layer 3

When the mutations in shared ERVs are examined, many are found to be identical to others. Just as will the distribution of ERVs, some shared mutations within a single shared ERV fall into nested hierarchies; some are shared by all, many by subsets of the whole, and each set falls within another set (Hughes & Coffin, 2005; Johnson and Coffin, 1999). Despite deviation caused by the same mechanisms effecting LTR-LTR discontinuity ratios, many of these nested hierarchies of mutation match those of distribution. Part of what makes this such powerful evidence for the evolutionary model is that is that ERV distribution and mutation rely on entirely different mechanisms; the function of integrase and the DNA replication complex, respectively. That the two nested hierarchies match at all is only explicable by common ancestry. The evidence for ERV ortholgoy is clear.

Summary

The three layers of ERV evidence that have just been laid out are as follows:

Layer 1: the presence of ERVs in identical loci among species of various degrees of taxonomic separation, and of the nested hierarchies they fall into.

Since they’re passed on through sexual reproduction, the many ERVs fixed in identical loci in different species necessitates the past presence of a species ancestral to both, that has since diverged into the two modern ones. And the patterns of their distribution indicate a specific sequence of divergence.

Layer 2: the comparative degrees of LTR-LTR discontinuity among full-length ERVs in identical loci.

Since LTRs are identical upon reverse transcription and subsequent insertion, greater divergence correlates to an older insertion. Thus the patterns of discontinuity indicate sequences of divergences consistent with those indicated by distribution.

Layer 3: shared mutations among ERVs identical loci and the corresponding nested hierarchies they fall into.

Since mutations accumulate and fix in populations of organisms, the distribution of shared mutation indicate a sequence of speciation events consistent with that which is indicted by both distribution and LTR-LTR discontinuity.


The majority of ERVs really did originate in a common ancestral species; most truly are orthologous.

Is this pattern ever violated and explained as a sequence becoming conserved by selection?

Yes, sometimes ERV integrations get resurrected in various mutational ways and become ORFan genes with important biochemical functions - and thus get included under purifying selection. This is very rare however, and does very little to deviate from the main pattern.

Again, occasional deviations from the main pattern are expected by a stochastic process. Again, the evidence for evolution from molecular phylogenetics is statistical in nature. Again, therefore, the evidence must be weighed probabilistically. Again, to falsify the pattern of common descent you would have to detect an incredible number of incongruent sites.

Just how strong is this main pattern? Let's take a look:

Amount of Shared ERVs

With so many claiming that it's only around 7 or 14, an important question is; just how many ERVs do humans share with chimpanzees? The answer is that humans and chimpanzees share virtually all of them. We know this is the case for two reasons; examination of indel variation, and whole-genome analysis.

Total Indel Variation

When lining up genomic sequences for comparison, there are many ways to measure difference. The most common is the measurement of substitutions; a base pair differing from one sequence to the next, such as an A, instead of a G. But an equally important measurement is that of indels:

An indel is a deletion or insertion of a sequence in an organism’s genome. When the genomes of multiple organisms are aligned, an indel in either genome will result in a gap. This is useful in determining the how many ERVs, Alus, or any other types of transposons are shared, since insertions at a given locus in only one lineage or only the other will result in gaps, yet insertions in identical loci leave no gaps:

The total length of all ~6.7 million transposable elements in the human genome is at least ~1.2 Gb (gigabases; billion base pairs), and the total length of all ~200 thousand ERVs is at least ~127 Mb (megabases; million base pairs) (International Human Genome Sequencing Consortium, 2001). But the total indel variation between the chimpanzee and human genomes is only ~3%, comprising a maximum of ~45 Mb (~1.5%) in each genome (Chimpanzee Sequencing and Analysis Consortium, 2005). Remember; that includes deletions and duplications, as well as the insertion of transposable elements, like ERVs. So only a fraction the ~45 Mb in the human genome could even potentially be ERVs in different loci. Even if every single ERV-sized indel in the human genome was an ERV at different loci between chimpanzees and humans, that would only represent a small fraction of the ~127 Mb of all ERVs; and a minute fraction of the ~1.2 Gb of all transposable elements. Thus, right from the start, we know that the majority of ERV are in identical loci.

Indel Variation Observed to Involve ERVs

Total indel variation provides a minimum number of transposable elements that can be shared in identical loci between chimpanzees and humans; but further examination is necessary to determine the actual number. One way this can be done is by isolating only the indels that are the right size to potentially be ERVs in different loci. Once this is done, the sequences corresponding to those gaps can be individually examined.

The results of such analysis are that less than 100 ERVs are human-specific (Polavarapu, Bowen, & McDonald, 2006). As previously stated, if a sequence is not only at a given locus in one lineage, nor only at a given locus in the other, then the only remaining possible state in which it can exist is at the same locus in both lineages. So the number of ERVs in identical loci is the total number minus the number that form gaps. With less than 100 of the ~200 thousand ERVs in the human genome yielding no gaps, the percentage of ERVs in identical loci is grater than 99.9%.


Whole-genome Analysis

In 2005, the available sequence of the Chimpanzee genome was aligned with that of the human genome, and an extensive comparison analysis was performed. As part of this analysis, the researchers looked at every available solo LTR and full-length ERV in the chimpanzee genome, and checked to see if there was also one at each corresponding locus. Just as with the examination of indels, the results were that less than 100 ERVs are human-specific and less than 300 ERVs are chimpanzee-specific (Chimpanzee Sequencing and Analysis Consortium, 2005; R. Waterston, personal communication, April 22, 2010).

In summary, indel variation shows that most transposable elements, such as ERVs, cannot be lineage-specific; they must be in identical loci. When the indels are examined, this is corroborated, and less than 0.1% of ERVs are found to be lineage-specific. Finally, definitive confirmation is obtained by genome-wide comparison, where virtually all ERVs are directly observed to be in identical loci.

Confirmed to an overwhelming degree.

In other words, homoplasy does not constitute the obstacle you're trying to pretend it is, and evolutionary biologists know how to control for it. The same basically goes for all the rest of the papers you link. Homoplasy can be detected through standard phylogenetic methods and distinguished from common descent.

Of course they know how to "control for it". In standard phylogeny, a homoplastic trait can become a homologous one and vice versa, if it is shown to help "resolve" a most "parsimonious" tree. Homoplasy is not detected in any objective sense of the word. It is statistically inferred, and can be arbitrarily reversed if it results in greater phylogenetic "resolution".

This doesn't even deserve a response, it's simply pulled out of you ass. It should be noteworthy even to yourself that you have to defend your position by simply making shit up in a conspiratorial fashion. The implications are pretty clear.

You can make shit up all day long, it's not going to make it a fact. This is simply an exposition into your personal paranoia about a scientific field you're psychoemotionally predisposed to dismiss out of hand before having properly educated yourself enough to fully understand.

I'm not making it up. That's how evolutionists actually think. Whenever something appears problematic for Evolution, even "astonishingly" unexpected from an evolutionary perspective, in the very next breath it is automatically absorbed as new evidence for how Evolution works. The literature is full of such examples.

Bla bla bla... :roll:

The problem is that you don't seem to understand that the evidence for evolution from molecular phylogenetics is statistical in nature. That means there's a pattern supported by a significant statistical weight that implies common descent. This pattern could technically easily be falsified, you would simply have to show that, on average, the number of sites divergent from the "main pattern" expected if common descent was true, were outweighing the number of sites congruent with common descent.

Give me a hypothetical example with specific animal groups. Don't just show me a picture of a spaghetti diagram and baldly assert that we should get those results if common descent is false.

A hypothetical example? Are you asking me to design you a hypothetical cluster of orthologous genes according to my own taste, for some arbitrary number of taxons, and then construct phylogenies from them and try to align all these trees and see if a central tree-like trend is produced? That would be a waste of time (besides being intensely laborious), because I can do much better.

Back in 2010 Douglas Theobald compared several sequence generating models in their ability to reproduce a pattern most similar to a known dataset.

Let's see how they each did:
http://www.nature.com/nature/journal/v465/n7295/abs/nature09014.html
http://theobald.brandeis.edu/pdfs/Theobald_2010_Nature_all.pdf
A formal test of the theory of universal common ancestry
Douglas L Theobald

Universal common ancestry (UCA) is a central pillar of modern evolutionary theory1. As first suggested by Darwin2, the theory of UCA posits that all extant terrestrial organisms share a common genetic heritage, each being the genealogical descendant of a single species from the distant past3, 4, 5, 6. The classic evidence for UCA, although massive, is largely restricted to ‘local’ common ancestry—for example, of specific phyla rather than the entirety of life—and has yet to fully integrate the recent advances from modern phylogenetics and probability theory. Although UCA is widely assumed, it has rarely been subjected to formal quantitative testing7, 8, 9, 10, and this has led to critical commentary emphasizing the intrinsic technical difficulties in empirically evaluating a theory of such broad scope1, 5, 8, 9, 11, 12, 13, 14, 15. Furthermore, several researchers have proposed that early life was characterized by rampant horizontal gene transfer, leading some to question the monophyly of life11, 14, 15. Here I provide the first, to my knowledge, formal, fundamental test of UCA, without assuming that sequence similarity implies genetic kinship. I test UCA by applying model selection theory5, 16, 17 to molecular phylogenies, focusing on a set of ubiquitously conserved proteins that are proposed to be orthologous. Among a wide range of biological models involving the independent ancestry of major taxonomic groups, the model selection tests are found to overwhelmingly support UCA irrespective of the presence of horizontal gene transfer and symbiotic fusion events. These results provide powerful statistical evidence corroborating the monophyly of all known life.

Here I report tests of the theory of UCA using model selection theory, without assuming that sequence similarity indicates a genealogical relationship. By accounting for the trade-off between data prediction and simplicity, model selection theory provides methods for identifying the candidate hypothesis that is closest to reality 16,17. When choosing among several competing scientific models, two opposing factors must be taken into account: the goodness of fit and parsimony. The fit of a model to data can be improved arbitrarily by increasing the number of free parameters. On the other hand, simple hypotheses (those with as few ad hoc parameters as possible) are preferred. Model selection methods weigh these two factors statistically to find the hypothesis that is both the most accurate and the most precise. Because model selection tests directly quantify the evidence for and against competing models, these tests overcome many of the well known logical problems with Fisherian null-hypothesis significance tests (such as BLAST-style Evalues) 16,21. To quantify the evidence supporting the various ancestry hypotheses, I applied three of the most widely used model selection criteria from all major statistical schools: the log likelihood ratio (LLR), the Akaike information criterion (AIC) and the log Bayes factor (LBF) 16,17.

...

All of the models examined here are compatible with multiple origins in both the above schemes, and therefore the tests reported here are designed to discriminate specifically between UCA and multiple ancestry, rather than between single and multiple origins of life. Furthermore, UCA does not demand that the last universal common ancestor was a single organism 24,25 ,in accord with the traditional evolutionary view that common ancestors of species are groups, not individuals 26. Rather, the last universal common ancestor may have comprised a population of organisms with different genotypes that lived in different places at different times 25 .
The data set consists of a subset of the protein alignment data from ref. 27, containing 23 universally conserved proteins for 12 taxa from all three domains of life, including nine proteins thought to have been horizontally transferred early in evolution 27. The conserved proteins in this data set were identified based on significant sequence similarity using BLAST searches, and they have consequently been postulated to be orthologues. The first class of models I considered (presented in Table 1 and Fig. 1) constrains all the universally conserved proteins in a given set of taxa to evolve by the same tree, and hence these models do not account for possible horizontal gene transfer (HGT) or symbiotic fusion events during the evolution of the three domains of life. Hereafter I refer to this set of models as ‘class I’. The class I model ABE, representing universal common ancestry of all taxa in the three domains of life and shown in Fig. 1a, can be considered to represent the classic three-domain ‘tree of life’ model of evolution 28.

...

For all model selection criteria, by statistical convention a score difference of 5 or greater is viewed as very strong empirical evidence for the hypothesis with the better score (in this work higher scores are better) 16,17 . All scores shown are also highly statistically significant (the estimated variance for each score is approximately 2–3). According to a standard objective Bayesian interpretation of the model selection criteria, the scores are the log odds of the hypotheses 16,17. Therefore, UCA is at least 10[sup]2,860[/sup] times more probable than the closest competing hypothesis. Notably, UCA is the most accurate and the most parsimonious hypothesis. Compared to the multiple-ancestry hypotheses, UCA provides a much better fit to the data (as seen from its higher likelihood), and it is also the least complex (as judged by the number of parameters).
The extraordinary strength of these results in the face of suspected HGT events suggests that the preference for the UCA model is robust
to the extent of HGT. To test this possibility, the analysis was expanded to include models that allow each protein to have a distinct, independent evolutionary history. I refer to this set of models, which rejects a single tree metaphor for genealogically related taxa, as ‘class II’. Representative class II models are shown in Fig. 2. Within each set of genealogically related taxa, each of the 23 universally conserved proteins is allowed to evolve on its own separate phylogeny, in which both branch lengths and tree topology are free parameters. For example, the multiple-ancestry model [AE1B] II comprises two clusters of protein trees, one cluster (AE) in which Archaea and Eukarya share a common ancestor but are genetically unrelated to another cluster (B) consisting only of Bacteria. Class II models are highly reticulate, phylogenetic networks that can represent very complex evolutionary mechanisms, including unrestricted HGT, symbiotic fusion events and independent ancestry of various taxa. Overall, the model selection tests show that the class II models are greatly preferred to the class I models.

The optimal class II models represent an upper limit to the degree of HGT, as many of the apparent reticulations are probably due to incomplete lineage sorting, hidden paralogy, recombination, or inaccuracies in the evolutionary models. Nonetheless, as with the class I non-HGT hypotheses, all model selection criteria unequivocally support a single common genetic ancestry for all taxa. Also similar to the class I models, the class II UCA model has the greatest explanatory power and is the most parsimonious.

...

The proteins in this data set were postulated to be orthologous on the basis of significant sequence similarity 27 . Because the proteins are universally conserved, all of the taxa have their own specific versions of each of the proteins. It would be of interest to know how the tests respond to the inclusion of proteins that are not universally conserved, as omitting independently evolved proteins could perhaps bias the results towards common ancestry. Nevertheless, the inclusion of bona fide independently evolved genes has no effect on the likelihoods of the winning class II models, except in certain cases to strengthen the conclusion of common ancestry (for a formal proof, see the Supplementary Information).

...

What property of the sequence data supports common ancestry so decisively? When two related taxa are separated into two trees, the
strong correlations that exist between the sequences are no longer modelled, which results in a large decrease in the likelihood. Consequently, when comparing a common-ancestry model to a multipleancestry model, the large test scores are a direct measure of the increase in our ability to accurately predict the sequence of a genealogically related protein relative to an unrelated protein. The sequence correlations between a given clade of taxa and the rest of the tree would be eliminated if the columns in the sequence alignment for that clade were randomly shuffled. In such a case, these model-based selection tests should prefer the multiple-ancestry model. In fact, in actual tests with randomly shuffled data, the optimal estimate of the unified tree (for both maximum likelihood and Bayesian analyses) contains an extremely large internal branch separating the shuffled taxa from the rest. In all cases tried, with a wide variety of evolutionary models (from the simplest to the most parameter rich), the multiple-ancestry models for shuffled data sets are preferred by a large margin over common ancestry models (LLR on the order of a thousand), even with the large internal branches. Hence, the large test scores in favour of UCA models reflect the immense power of a tree structure, coupled with a gradual Markovian mechanism of residue substitution, to accurately and precisely explain the particular patterns of sequence correlations found among genealogically related biological macromolecules.

This is fucking GAME OVER for anything but common descent.

Such tests have been done on some of the most difficult organisms to infer phylogenies from (fast-evolving single-celled organisms prone to horizontal gene transfer), using large clusters of genes and producing multiple aligments.
See for example tests such as this:
http://www.biomedcentral.com/1741-7007/11/46
Seeing the Tree of Life behind the phylogenetic forest
Pere Puigbò, Yuri I Wolf and Eugene V Koonin*
Although the FOL includes very few trees with exactly identical topologies, we found that the topologies of the trees were far more congruent than expected by chance.

.

More congruent than expected by chance? What exactly does this mean? If genomes were randomly assembled all at once?

It means that if you took their total dataset, constructed all possible trees from the dataset, then randomly chose some small portion of them and tried to align them, the odds that you'd just so happen to pick a set that statistically converge on the same overall tree-like trend is extremely improbable. Nevertheless, this is what they observe, meaning there's some kind of reason this pattern exists. Can you guess what it is?

(There are many studies like this one that all conclude basically the same thing). This underscores what tried to explain above, there is a singificant statistical weight in favor of tree-like descent, even when all the confounding factors are included. The number of sites congruent with the nested hierachy expected from common descent STILL significantly outweighs the number of divergent sites. The most plausible and simples explanation for this observation is common descent. This could have been different, the trees could have disagreed more than they could have converged, and they could have disagreed to an extremely high statistical degree. But they DON'T, they do the opposite. Common descent is therefore still massively statistically attested.

There is a deep flaw in this reasoning, and that is the metaphysical assumption that only common descent can explain nested hierarchies. Without explanation, you demand that trees should be a chaotic mess if Common Descent is false. Why? What's your reasoning?

Do you believe we should observe wildly discordant things like Dogs grouping with Termites and Whales grouping with Pine Cones if common descent is false?

I've already responded to this in the other thread. Only evolution can truly make sense of the observed pattern.

Basically, yes. The twin nested hierarchies we observe are not expected on any other hypothesis than common descent. Not even using the laughably ad-hoc rationalization that "the designer re-used older designs". (As explained in the other thread).

But seriously. Why do designers re-use older designs anyway, instead of just designing entirely new ones from the ground up? Oh yeah, constraints on time, resources and creativity(individual human beings are only so creative). Is your postulated supernatural and omnipotent designer constrained by time, resources and creativity? Hmmm.....

This very same fact is true for ERV's, the number of sites shared due to common descent significantly outweighs the number of sites shared due to homoplasies.

What is your objective criteria for distinguishing homology vs. homoplasy?

Already explained earlier in this post with references.

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

.....But the first problem with the idea that this renders uncommon ancestry plausible is that there are ERVs shared by many more than just two lineages. For instance, there are ERVs shared by chimpanzees, humans, gorillas, orangutans, gibbons, and Old World Monkeys (Kurdyukov et al., 2001; Lebedev et al., 2000). The second problem—and by far, the most important—is that we do not share only a few ERVs in identical loci with Chimpanzees; examination of indel variation, and whole-genome analysis shows that we share virtually all of them with Chimpanzees. This is discussed extensively in the "Amount of Shared ERVs" section, above.

This is a strawman as I never made the argument that the pattern of shared ERV insertions could be explained by the odds, or by chance. (I believe this is known as the Birthday Paradox)

My argument is that there is evidence of highly insertion-site-specific integration mechanisms. And many researchers have admitted they know very little about how the integration process actually works. There is a progressive pattern of discovering less and less randomness to the process then was previously assumed, even down to identical nucleotide insertions.

Evolutionists are assuming the integration sites could not be that specific. If it happens, it is rare. How do you know it is rare?

Already explained why this is irrelevant, since individual orthologous loci can be compared by sequence.

There's another problem with the design hypothesis. The vast majority of these ERV insertions are junk. They do nothing. Why would a designer fill up the genomes of large multicellular eukaryotes with mutationally degrading reverse-transcriptase genes and it's associated but also mutationally degrading promoter regions? Why would your mysterious designer shovel them into the genomes of his creations in a pattern that implies common descent to such an overwhelming degree? It simply doesn't make sense.

And then there's the fact that we've never seen the designer operate and "do creations". In contrast, we can see evolution happening in the here and now. All the mechanisms of evolution are observed facts, as also explained in the other thread.

Since these ERV's are also mostly junk, they are evolving at a neutral rate, accumulating mutations over time. As speciation events happen further and further back in time, even single ERV sites shared between multiple species accumulate mutations such that the pattern you get when doing sequence alignments from their sites still produce a nested hierarchy congruent with common descent.

References please.

Given above in this post.

And if by contrast, sequences do not appear to be "evolving" at a neutral rate, why can't the evolutionist simply infer that they must have contributed to fitness and conserved by selection? They could be highly conserved in one specific lineage, and neutral in another, in order to explain any pattern of rate of change in sequence alignment.

Sure, you could rationalize the observation in this way, but you'd be proposing a more complicated model that doesn't really make sense.
Say for example you observe some orthologous ERV insertion distribututed in multiple species. When you compare the sequences, you see they diverge increasingly and you can construct a classic distance-based tree. Okay, you say, I simply rationalize that the two most similar sorthologues have been constrained by natural selection - the 3rd most close orthologue has lost purifying selection (or selection is less constrained) - the 4th most close orthologue is even less constrained (or purifying selection got deactivated even longer ago) and so on and so forth until you have rationalized all the orthologues with increasingly relaxed purifying selection/deactivation time of selection.

This is a much more complicated model with less explanatory power. There's no a priori reason to expect such a pattern of increasinly relaxed selective pressures for each and every species. No single overall framework seems able to predict this mechanism, it is for all intents and purposes only a rationalization. We haven't even observed this effect in nature etc. etc. one could go on about occams razor and what not, in addition to the statistical unlikelyhood of finding just such a pattern.

In contrast a single predictive theory with mechanistic explanatory power makes perfect sense of the pattern.

 

[Rumraket]

This is the problem with unconstrained rationalizations, they can be bend to fit anything. If you just throw statistical tests out the window, take a dump on occam's razor, don't bother with observational justification when doing inferences, or with making testable predictions, then you can make anything fit in an ad-hoc manner.

The design assertion cannot be observationally falsified. Anything we observe you can simply respond "is what the designer wanted to design".

As I have amply demonstrated, actual constraints are being employed with respect to evolutionary inferences. They're statistical in nature, meaning there's actual quantifiable relationships involved that can be resolved mathematically and used to accept or reject certain hypotheses. There's this entire branch of mathematics, you may have heard of it, it's called STATISTICS AND PROBABILITY THEORY.

Evolution also works only and exclusively with the observed. No mechanisms are being postulated that haven't actually been observed in the present. Particularly important is that these mechanisms must make testable predictions (such as certain patterns being present to some specific statistical extend).

 

[Deleted member 619]

I have spent the past few days searching the literature

There's your problem, then. What you really need to do is to spend years studying the literature and the principles behind it. Spending merely a few days in search of citations that appear to support magic is not study, it's apologetics.

Evolution is an observed fact. Your pathetic masturbation fantasy is bollocks. Deal with it.

 

[herebedragons]

Good post Rumraket. I am not very familiar with the details, just the general, overall concepts, nor do I have time to flesh all of that out. So your posts were a great extension and support for my points.

However, you missed an important quote from Theobald

According to a standard objective Bayesian interpretation of the model selection criteria, the scores are the log odds of the hypotheses16,17. Therefore, UCA is at least 10e2,860 times more probable than the closest competing hypothesis. Notably, UCA is the most accurate and the most parsimonious hypothesis. Compared to themultiple-ancestry hypotheses,UCAprovides a much better fit to the data (as seen from its higher likelihood), and it is also the least complex (as judged by the number of parameters).

ABE: (oops, sorry, I just realized you didn't actually miss this quote, but I want to highlight it anyway)

That is a likelihood of something like 30 times the number of atoms in the observable universe! But hey, [sarcasm]not absolute proof[/sarcasm].

Of course, this paper is very hard to understand, so it will most likely just be dismissed as scientific voodoo.

Another thing to note, they did not test all possible origin hypotheses, just ones based on an evolutionary model. This is why I insist that creationists propose a model that can be tested. Perhaps they could propose a model that fits the evidence 10e2860 times better than UCA. But without a working model it is just "what-ifs" and incredulity; nothing science can actually work with.

HBD