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Author Topic:   Why are there no human apes alive today?
Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


Message 976 of 1075 (626091)
07-27-2011 3:21 AM
Reply to: Message 969 by Taq
07-26-2011 7:12 PM


Re: Moderator Advisory
Taq says
So even your poster child PTERV-1 insertions are not found at the same position in each genome. HIV does not insert into the same position each time it inserts. Your argument is a complete failure at this point.
If you can not find a single example of a virus that inserts into the same position each and every time it inserts then the evidence above stands. You can not claim that the orthologous insertions can best be explained by independent insertions.
I would ask that your response to this post should focus on retroviral insertion alone, and not anything else. In this way we can move in a straighter path towards the topic and keep the admins happy.
Taq, I'll try to focus when I stop laughing!. I think you have validated my assertion that ERV's as support for common descent are fairytales.
Nuggin says...
"Further, you have REPEATED your false claim that these things are inserted in "similar" places. Not similar. The SAME."
Before we can move on I need Taq, and Nuggin to make up their minds. I am replying to your post this time Taq. What is the proof that ERV's are proof of common ancestry..is it that the ghosts of ERV's are found in the exact same position in the genome such that it would defy chance or is that they are scattered everywhere willy nilly and this proves common descent?
I however know that what Nuggin is proposing is in fact what your researchers cite as evidence for common descent ie the ghost relic remnant in the exact same place, when it happens, is meant to prove common descent beyond irrefuteability.
So Nuggin here you go. Here is a reseach paper that suggests 95.5% of ERV's are in non-orthologous regions. Hence not inherited. This paper speaks to horizontal gene transfer in relation to ERV's. So just like I said a mossie likely bit them all or they sneezed on each other, is all these ERV's show.
So when an ERV is placed in a similar spot in two species this proves common descent. When it doesn't this means it just got there some other way. It seems ERV's are unfalsifiable.
When ERVs show no common descent your scientists invent some theory to explain it like it got there via HGT or bla. If the ERV has a bias for some spot in the genome then this is irrefuteable proof of descent and any other ERV in the wrong place is explained away.
"We unambiguously map 287 retroviral integration sites and determine that approximately 95.8% of the insertions occur at non-orthologous regions between closely related species. Phylogenetic analysis of the endogenous retrovirus reveals that the gorilla and chimpanzee elements share a monophyletic origin with a subset of the Old World monkey retroviral elements, but that the average sequence divergence exceeds neutral expectation for a strictly nuclear inherited DNA molecule. Within the chimpanzee, there is a significant integration bias against genes, with only 14 of these insertions mapping within intronic regions. Six out of ten of these genes, for which there are expression data, show significant differences in transcript expression between human and chimpanzee. Our data are consistent with a retroviral infection that bombarded the genomes of chimpanzees and gorillas independently and concurrently, 3—4 million years ago. We speculate on the potential impact of such recent events on the evolution of humans and great apes."
Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans | PLOS Biology
So Taq, would you like to repost or shall I try to reply seriously to this post of yours.
Edited by Mazzy, : No reason given.

This message is a reply to:
 Message 969 by Taq, posted 07-26-2011 7:12 PM Taq has replied

Replies to this message:
 Message 977 by Larni, posted 07-27-2011 5:11 AM Mazzy has not replied
 Message 979 by Taq, posted 07-27-2011 11:27 AM Mazzy has replied

Larni
Member (Idle past 164 days)
Posts: 4000
From: Liverpool
Joined: 09-16-2005


Message 977 of 1075 (626095)
07-27-2011 5:11 AM
Reply to: Message 976 by Mazzy
07-27-2011 3:21 AM


Re: Moderator Advisory
Article writes:
An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists [29]. This seems unlikely in light of the extensive molecular evolutionary data that have been collected over the last few years [5,25] that clearly place orangutan as the outgroup species to the human—chimpanzee—gorilla clade and Old World monkeys as an outgroup to the human/ape lineage.
Article writes:
Several speculative scenarios may be envisioned to explain the absence of retrovirus in both the orangutan and human lineages. It is possible that the African apes evolved a susceptibility, or humans and Asian apes developed resistance to infection, although in either scenario convergent evolution would have had to have occurred with respect to the viral infections. Studies of the retroviral infection of the Lake Casitas mouse population reveal that such susceptibility/resistance genes may emerge very quickly among closely related strains of mice [34]. Another scenario may be that the lineage that ultimately gave rise to humans did not occupy the same habitat as the ancestral chimpanzee and gorilla lineages. An excursion by early hominids to Eurasia during the time that PTERV1 infected African great apes and then a return to Africa would explain this phylogenetic inconsistency. It is also possible that this effect may have been created by dramatic differences in ancestral population structure. If, for example, the ancestral populations of humans and orangutans were substantially larger than those of the African great apes, the fixation of new insertions (1/2N) would occur much more rapidly within small inbred populations even if similar infection rates existed. A similar model has recently been proposed, albeit in the opposite direction, to explain an increase of apparent Alu Ya5 and Yb8 retroposition activity in the human lineage but not in chimpanzees and gorillas [35]. In this regard, it is interesting that documented differences in the patterns of endogenous retrovirus between domesticated and feral species have been attributed to inbreeding [19,20]. There is, however, no evidence to date that the ancestral populations of chimpanzees were smaller than that of humans. Recent studies suggest that ancestral chimpanzee populations, in fact, may have been two to four times larger [36,37] than the effective human population size (greater than 10,000). A dramatic population crash in ancestral gorilla and chimpanzee populations would be required to explain the effect we have observed. Further population genetic studies of contemporary great apes or paleoanthropological work may help to eliminate these and other possible scenarios.
Did you forget to read the discussion?
Edited by Larni, : Second paragraph

This message is a reply to:
 Message 976 by Mazzy, posted 07-27-2011 3:21 AM Mazzy has not replied

Portillo
Member (Idle past 4161 days)
Posts: 258
Joined: 11-14-2010


Message 978 of 1075 (626096)
07-27-2011 5:16 AM
Reply to: Message 973 by Admin
07-26-2011 8:31 PM


Re: Repeating the Topic
quote:
Also think how Mazzy must feel going it alone against several evolutionists with none of them conceding any of her points. You're not the only one experiencing feelings of frustration.
Thats a great point. And lets not forget that this is a Creation vs Evolution forum. Not just an evolution forum!
Edited by Portillo, : No reason given.

This message is a reply to:
 Message 973 by Admin, posted 07-26-2011 8:31 PM Admin has seen this message but not replied

Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 979 of 1075 (626133)
07-27-2011 11:27 AM
Reply to: Message 976 by Mazzy
07-27-2011 3:21 AM


Re: Moderator Advisory
Before we can move on I need Taq, and Nuggin to make up their minds. I am replying to your post this time Taq. What is the proof that ERV's are proof of common ancestry..is it that the ghosts of ERV's are found in the exact same position in the genome such that it would defy chance or is that they are scattered everywhere willy nilly and this proves common descent?
Before I can explain why ERV's can be used to evidence common ancestry you need to agree that retroviruses insert randomly amongst billions of insertion sites. Until we have an agreement on how retroviruses insert into the genome we can not proceed.
Now to highlight more of your mistakes.
Here is a reseach paper that suggests 95.5% of ERV's are in non-orthologous regions.
False. It says that 95.5% of PTERV-1 insertions are not within 160,000 base pairs of each other, the resolution of the BAC clone technique that the authors are using. It does not say that 95.5% of ALL ERV's are non-orthologous. They are looking at PTERV-1 insertions specifically which are a subset of all ERV's.
So when an ERV is placed in a similar spot in two species this proves common descent. When it doesn't this means it just got there some other way. It seems ERV's are unfalsifiable.
False. An orthologous ERV indicates that the insertion happened once in a common ancestor. A non-orthlolous ERV indicates the opposite, that the insertion occurred independently in both lineages.
The way to falsify the ERV data is to show that:
1. Orthologous ERV's do not produce a single nested hierarchy.
2. LTR divergence greatly differs from the tree created through orthologous loci.
3. Overall ERV divergence differs from the two trees above.
So Taq, would you like to repost or shall I try to reply seriously to this post of yours.
You do realize that there are more than PTERV-1 insertions in these genomes? You do know that PTERV-1 and HERV-K are different, don't you?
Edited by Taq, : No reason given.

This message is a reply to:
 Message 976 by Mazzy, posted 07-27-2011 3:21 AM Mazzy has replied

Replies to this message:
 Message 982 by Mazzy, posted 07-27-2011 1:48 PM Taq has replied

Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


Message 980 of 1075 (626150)
07-27-2011 1:13 PM
Reply to: Message 971 by Taq
07-26-2011 7:19 PM


Listen Taq. I am tired of your belittling remarks. Your recent ERV fiasco gives me plenty of legs to retaliate. It is not I that wears the cap of ignorance for this week.
Taq says
It does comport. In fact, it comports quite nicely. None of the PTERV-1 insertions are orthologous as one would expect if the consensus phylogenies are accurate. That you fail to understand this only highlights your ignorance.
The article plainly states 'DOES NOT COMPORT', If you disageee you should call the researchers up and tell 'em what's what, according to Taq.
It also says
"When a retrovirus reproduces, identical copies of LTR sequences are created on either side of the retroviral element; the divergence of LTR sequences within a species can be used to estimate the age of an initial infection. Eichler and colleagues estimate that gorillas and chimps were infected about 3-4 million years ago, and baboon and macaque about 1.5 million years ago. The disconnect between the evolutionary history of the retrovirus and the primates, the authors conclude, could be explained if the Old World monkeys were infected by "several diverged viruses" while gorilla and chimpanzee were infected by a single, though unknown, source."
As for how this retroviral infection bypassed orangutans and humans, the authors offer a number of possible scenarios but dismiss geographic isolation:
http://www.sciencedaily.com/...ases/2005/03/050328174826.htm
It is therefore not vertical Mendelian inheritable transmission of this ERV but in this case it was horizontal. Hopefully you understand the difference. What it means is that your researchers appear to have no clue what they are seeing in these ghosts of so called relics and are lost in their excuses to maintain the status quo.
ERV's can be used equally well to demonstrate NO ancestry to chimps just as well as they show otherwise. This is called picking and choosing and evoutionary science is full of it. PTERV-1 demonstrates simply that mankind is not related to chimps... and should be the end of the story. But rather more convoluted excuses in the form of theories ensue and this makes it all OK for you.
These excuses only make it OK in the minds of faithful TOE suppporters. I and others, as thinking and reasoning beings can see what you actually have is no definitive evidence at all in using ERV's. It is yet another 'pull a rabbit out of the hat time' when needed, but leave the goose and other contradictions in the hat unseen.
When evidence provides a refute and falsification to the concept of ERV's informing ancestry is addressed with pages of vague excuses, maybe's and perhaps or they don't know. Whenever your theory is falsified more theories come along to save the day eg gradual change vs punctuated equilibrium, and there are plenty more of them.
If you are trying to prove there were intermediates between ape and mankind, ERV's are not going to do it for you. However I can respect your views on ERV's as a matter of faith.

This message is a reply to:
 Message 971 by Taq, posted 07-26-2011 7:19 PM Taq has replied

Replies to this message:
 Message 981 by Taq, posted 07-27-2011 1:25 PM Mazzy has not replied

Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(1)
Message 981 of 1075 (626154)
07-27-2011 1:25 PM
Reply to: Message 980 by Mazzy
07-27-2011 1:13 PM


The article plainly states 'DOES NOT COMPORT', If you disageee you should call the researchers up and tell 'em what's what, according to Taq.
You are ignoring the context. The PTERV-1 insertions would not comport IF THEY WERE FOUND AT ORTHOLOGOUS POSITIONS. That is why the authors went to so much trouble to find the genomic locus for all of the PTERV-1 insertions. What did they find? PTERV-1 ERV's are NOT FOUND AT ORTHOLOGOUS POSITIONS, therefore they do comport with the consensus phylogeny. Notice the title of the paper? See that part that says "Lineage Specific"?
Getting back on track, do we have agreement that retroviruses insert randomly amongst millions to billions of insertion sites? As soon as we agree on this well evidenced point we can move to the next part of my explanation of why ERV's can be used to evidence common ancestry.

This message is a reply to:
 Message 980 by Mazzy, posted 07-27-2011 1:13 PM Mazzy has not replied

Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


Message 982 of 1075 (626157)
07-27-2011 1:48 PM
Reply to: Message 979 by Taq
07-27-2011 11:27 AM


Re: Moderator Advisory
Taq says
Before I can explain why ERV's can be used to evidence common ancestry you need to agree that retroviruses insert randomly amongst billions of insertion sites. Until we have an agreement on how retroviruses insert into the genome we can not proceed.
Ok ..I'll go along. Let's say ERv's insert randomly. What's next?
False. It says that 95.5% of PTERV-1 insertions are not within 160,000 base pairs of each other, the resolution of the BAC clone technique that the authors are using. It does not say that 95.5% of ALL ERV's are non-orthologous. They are looking at PTERV-1 insertions specifically which are a subset of all ERV's.
It also says
"We unambiguously map 287 retroviral integration sites and determine that approximately 95.8% of the insertions occur at non-orthologous regions between closely related species."
"Our data are consistent with a retroviral infection that bombarded the genomes of chimpanzees and gorillas independently and concurrently, 3—4 million years ago. We speculate on the potential impact of such recent events on the evolution of humans and great apes."
What are you arguing about? Are you suggesting that every virus becomes an endogenous retrovirus.? This research is informing the fact that some retrovirus are non-orthologous, meaning not where it should be if it was inherited. The other thing demonstrated is that chimps are not related to mankind and researchers need a plethora of excuses to justify this ERV not being found in chimps, as expected.
I'd say some virus have a preference bias for particula genomic sites. Hence they end up in the same region due to preference and not ancestry.
False. An orthologous ERV indicates that the insertion happened once in a common ancestor. A non-orthlolous ERV indicates the opposite, that the insertion occurred independently in both lineages.
The way to falsify the ERV data is to show that:
1. Orthologous ERV's do not produce a single nested hierarchy.
2. LTR divergence greatly differs from the tree created through orthologous loci.
3. Overall ERV divergence differs from the two trees above.
and why are you reiterating what I said. I have stated all along that ERV's could be the result of something like a mossie bite, not common descent. I think it is pre conceived assumptions alone that prescribe if an ERV is ancestral or horizontally transfered. Let's remember they are looking for ghost remnants of virus that I expect continued to evolve. How on earth would they know what they are seeing? It is the presumption of ancestry that is the driving force re ERV's?
You do realize that there are more than PTERV-1 insertions in these genomes? You do know that PTERV-1 and HERV-K are different, don't you?
Yes I do. However it takes just one example to falsify a theory and open the door to Alice in Wonderland.
Let's get on with the lesson as to how randomly inserted ERV's end up being conclusive proof for common descent with apes.

This message is a reply to:
 Message 979 by Taq, posted 07-27-2011 11:27 AM Taq has replied

Replies to this message:
 Message 983 by Taq, posted 07-27-2011 2:49 PM Mazzy has replied

Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(1)
Message 983 of 1075 (626171)
07-27-2011 2:49 PM
Reply to: Message 982 by Mazzy
07-27-2011 1:48 PM


Re: Moderator Advisory
Ok ..I'll go along. Let's say ERv's insert randomly. What's next?
We then calculate the probability of two retroviruses inserting into the same position in two genomes. Given that there are millions to billions of bases where these retroviruses can insert into the chances of this happening multiple times in multiple species is in the range of winning the Powerball lottery several times in a row. Do you agree with this?
Added by edit: Just thought I would do the math for you. Let's say that a virus has 1 million possible insertion sites (which is a VERY low numer, so I am erring in your favor). This means that, on average, there will be one orthologous insertion out of every 1 million independent infections. Just one. So how many ERV's do we need in order to see 10 orthologous ERV's? That would be 1 in 1 million to the 10th power or 1 to 1E60 (thats a one with 60 zeros after it), and that is just for 10 orthologous ERV's.
Are we agreed on these figures?
Now to clean up your understanding of the PTERV-1 paper which will become important later on.
It also says
"We unambiguously map 287 retroviral integration sites and determine that approximately 95.8% of the insertions occur at non-orthologous regions between closely related species."
Again, context is everything. Retroviral integration sites of which virus? What probe did they use for BAC clone selection?
The answer is that they used a PTERV-1 specific probe to select for the large chunks of genomic DNA that contained PTERV-1 insertions, and PTERV-1 insertions only. Their methodology would not have picked up HERV-K or HERV-W insertions, to use two examples. That 95.5% figure is for PTERV-1 ERV's (within the resolution of 160 kb BAC clones), not for all ERV's as you suggested before.
"Our data are consistent with a retroviral infection that bombarded the genomes of chimpanzees and gorillas independently and concurrently, 3—4 million years ago. We speculate on the potential impact of such recent events on the evolution of humans and great apes."
What led them to this conclusion? The fact that PTERV-1 insertions were found at non-orthologous locations, along with sequence divergence data.
I'd say some virus have a preference bias for particula genomic sites. Hence they end up in the same region due to preference and not ancestry.
It only took you 4 paragraphs to go back on your word. Go figure.
This discussion can not go forward if you are going to go back on your word. Either agree that retroviral insertions are random or that they are directed to specific locations. Pick one, and we will discuss further.
I have stated all along that ERV's could be the result of something like a mossie bite, not common descent.
You have around 200,000 ERV's in your genome. Are you telling me that all of those ERV's are due to infections that you acquired during your lifetime? At the same time, your parents and sibilings have these very same ERV's in their genomes. Did your parents and siblings also suffer these same infections, and did those same infections result in identical insertions at identical positions in their genomes?
Edited by Taq, : No reason given.

This message is a reply to:
 Message 982 by Mazzy, posted 07-27-2011 1:48 PM Mazzy has replied

Replies to this message:
 Message 987 by Mazzy, posted 07-27-2011 6:23 PM Taq has replied

Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


(1)
Message 984 of 1075 (626178)
07-27-2011 3:36 PM
Reply to: Message 974 by Taq
07-26-2011 8:37 PM


Re: Repeating the Topic
Taq says
I am only replying to clarify my own posts and how it relates to the topic. I plan to show that ERV's do group humans with the rest of the apes. To do this, we first have to establish a working knowledge of how ERV's insert into genomes. Mazzy has made claims about retroviral insertion that are just plain wrong. If I am to show that ERV's do group humans with other apes I have to clear up the misinformation concerning ERV insertion. If that part of the discussion does drag on I will be happy to move the discussion to a different thread.
In fact, all you will be doing is entertaining me with the flavour of the month and how to avoid addressing inconsistencies or ignoring them. It is you that is just plain wrong and can talk the talk of avoidance and recognition of evolved ghosts.
It is simply a fact that one example of inconsistecy or contradiction should falsify any theory. I have produced one example and more. To proffer excuses as to why there is inconsistency does not deny a concept has been falsified.
It is easy for an evolutionists to alledge Mazzy provides no basis for her arguments, when clearly evolutionists are are the ones that cannot privide a basis for inconsistencies with any more than hand waving. You are NOT proving facts. You are proving theory to support theory. You are grasping onto strands of staw and ignoring the fire igniting beneath your claims that has burned this concept to the ground.
Here is another example.
"Why would a deletion occur randomly in the exact same place in the Guinea Pig and the Primate? Obviously this is not evidence of common descent since the two lineages are so separated. So what is it evidence of? This suggests that these deletions are non-random, perhaps part of a regulatory mechanism, which is more aptly described as engineering mechanisms rather than with neo-darwinian mechanisms.
ERVs are also considered to be strong evidence of common descent by Neo-Darwinists. These are thought to be fossilized remnants of ancient retro-viral infections which make marks in the genome at the exact same locations for Humans, Chimps and Gorillas, thus provig a common ancestor.
Dr Sean Pitman discusses the problems with using ERV's as proof of neo-Darwinism. One problem is the presence of other ERV's in the chimp and gorilla genome which are NOT Present in the human genome. If ERV's can be used to prove a common ancestor, then they can also be used to DISprove a common ancestor. It turns out that many of the basic assumptions underlying the ERV thinking has been found to be incorrect. Insertions are not random, but are related to HOT SPOTS. And rather than being non-functional, they seem to be involved in highly important regulatory functions.
Bottom line is that neo-Darwinism has actually been retarding progress in molecular biology research by either making false predictions, or preventing research into fertile areas. One of these impediments was the 25 year insistance on non-coding JUNK DNA which we now know was a false prediction by neo-Darwinism and impediment to research."
http://open.salon.com/...vs_evolution_and_intelligent_design
and
http://www.iscid.org/...rs/Borger_SharedMutations_061506.pdf
So why does a guinea pigs have the same ERV in the same spot and not be closely related? Do you think convoluted, complicated riddles and excuses resolves this dilemma for you? It does not.
Here is just on other example that falsifies ERV's as being irrefuteable evidence of ancestry and yet another time that a plethora of maybe's and porobably's will ensue to save the day and your theory.
*How about we progess no further untill you explain 1. how PtERV1 is found in African great apes but not human and 2. how a guinea pig has the same ERV in the exact same region as a human but is not closely related.*
Let's see just who ignores points or is unable to profer robust evidence to save the day but would rather prattle on with what suits them.
If you are unable to answer these points then I would say you have no basis to speak to any of it. To take only what agrees with your theory and ignore the inconsistencies without addressing them with scientific evidence as far as I am concerned is just not good enough for a person that does not consider themselves to be an ape.
BTW thanks Larni and Portillo. Yes it is frustrating when my points are totally ignored. There are many evos here and just me towing my line. You are both correct in pointing out that many evolutionary researchers have huge concerns about primate phylogeny. However it is only ever creationists that are stupid and ignorant for saying so, apparently.
One example is sufficient to falsify a theory. As far as I am concerned ERV's have been falsified as being used as a consistent determiner of ancestral relationships. All that can be provided is straw grabbing and picking and choosing what suits at this time and excuses for the rest.
However I am interested in the lesson from you Taq. The more I understand the better I can refute at that level.
Edited by Mazzy, : No reason given.

This message is a reply to:
 Message 974 by Taq, posted 07-26-2011 8:37 PM Taq has replied

Replies to this message:
 Message 985 by Taq, posted 07-27-2011 4:07 PM Mazzy has replied

Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(1)
Message 985 of 1075 (626183)
07-27-2011 4:07 PM
Reply to: Message 984 by Mazzy
07-27-2011 3:36 PM


Re: Repeating the Topic
It is simply a fact that one example of inconsistecy or contradiction should falsify any theory. I have produced one example and more.
In order for me to address this claim we first need to agree on the basics of retroviral insertion.
Above, I made a calculation for the probability of getting 10 orthologous insertions. Do you agree with these calculations or not?
Added by edit:
*How about we progess no further untill you explain 1. how PtERV1 is found in African great apes but not human and 2. how a guinea pig has the same ERV in the exact same region as a human but is not closely related.*
PTERV-1 was species specific and these infections occurred after the different lineages branched of of their common ancestors. The fact that retroviruses continue to infect species does not, in any way, refute the fact that orthologous ERV's are inherited from a common ancestor. If humans do not share a common ancestor with other apes then you should not find a single orthologous ERV, but instead you find tons of them.
You might as well try to refute the argument that French and Spanish share a common ancestral Latin language by pointing to the differences between the languages, forgetting that it is the commonalities that point to their common ancestral language.
Also, the pages you linked to talked about the GULO pseudogene. This is not an ERV.
Edited by Taq, : No reason given.
Edited by Taq, : No reason given.
Edited by Taq, : No reason given.

This message is a reply to:
 Message 984 by Mazzy, posted 07-27-2011 3:36 PM Mazzy has replied

Replies to this message:
 Message 986 by Panda, posted 07-27-2011 6:09 PM Taq has not replied
 Message 988 by Mazzy, posted 07-27-2011 6:36 PM Taq has replied

Panda
Member (Idle past 3713 days)
Posts: 2688
From: UK
Joined: 10-04-2010


Message 986 of 1075 (626208)
07-27-2011 6:09 PM
Reply to: Message 985 by Taq
07-27-2011 4:07 PM


Re: Repeating the Topic
Edited by Admin, : Hide off-topic comments.

This message is a reply to:
 Message 985 by Taq, posted 07-27-2011 4:07 PM Taq has not replied

Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


Message 987 of 1075 (626209)
07-27-2011 6:23 PM
Reply to: Message 983 by Taq
07-27-2011 2:49 PM


Re: Moderator Advisory
Taq said
We then calculate the probability of two retroviruses inserting into the same position in two genomes. Given that there are millions to billions of bases where these retroviruses can insert into the chances of this happening multiple times in multiple species is in the range of winning the Powerball lottery several times in a row. Do you agree with this?
Added by edit: Just thought I would do the math for you. Let's say that a virus has 1 million possible insertion sites (which is a VERY low numer, so I am erring in your favor). This means that, on average, there will be one orthologous insertion out of every 1 million independent infections. Just one. So how many ERV's do we need in order to see 10 orthologous ERV's? That would be 1 in 1 million to the 10th power or 1 to 1E60 (thats a one with 60 zeros after it), and that is just for 10 orthologous ERV's.
Are we agreed on these figures?
No. If we are talking about PTERV-1, it was not found in the right spot in humans nor orangs so these calculations do not apply to how amazing it was for PTERV-1 to reside in a particular exact spot of the human and chimp genome. WHY? because it wasn't found where it should be, much to the surprise of the researchers who have offered excuses for same.
I'll agree your researchers like to play with algorithms that are searching for ghosts.
If you want to demonstrate the magic of it all why don't you use an ERV that actually connects a chimp to a human.
Again, context is everything. Retroviral integration sites of which virus? What probe did they use for BAC clone selection?
The answer is that they used a PTERV-1 specific probe to select for the large chunks of genomic DNA that contained PTERV-1 insertions, and PTERV-1 insertions only. Their methodology would not have picked up HERV-K or HERV-W insertions, to use two examples. That 95.5% figure is for PTERV-1 ERV's (within the resolution of 160 kb BAC clones), not for all ERV's as you suggested before.
They can construct their models to pick up what they want, the point is they did not pick up PTERV-1 in the human and orang where it should be if it was inhereted, thereby falsifying the validity of any ancestral connection between chimps and humans. That is what this research plainly demonstrates. Excuses and more hypothesis to hand wave it away is not what I would call valid irrefuteable science.
What led them to this conclusion? The fact that PTERV-1 insertions were found at non-orthologous locations, along with sequence divergence data.
These insertions were not found in humans or ornags in such a way as to demonstrate close ancestry. Do you think your researchers are telling porkies? PTERV1 and the rest were not found in certain spots..meaning they were not inherited but were gained through HGT or other way. As for how this retroviral infection bypassed orangutans and humans, the authors offer a number of possible scenarios. Whatever conclusions that are made of this are based on predetermined assumptions of what is related to what and this becomes a part of the insertion values in any model.
"And knowing how these retroviral elements infiltrated some apes while sparing others could provide valuable insights into the process of evolution itself." .....
Simply means they have no clue.
http://www.sciencedaily.com/...ases/2005/03/050328174826.htm
It only took you 4 paragraphs to go back on your word. Go figure.
This discussion can not go forward if you are going to go back on your word. Either agree that retroviral insertions are random or that they are directed to specific locations. Pick one, and we will discuss further.
Read this
"Thus, 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."
http://www.plosbiology.org/article/infooi/10.1371/journal.pbio.0020234
WOW!...Integration site preferences as I mentioned...Go figure!
My word meant I would go along for the purpose of this discussion. That does not also mean that I accept any of it as factual. Do not be confused about this.
You have around 200,000 ERV's in your genome. Are you telling me that all of those ERV's are due to infections that you acquired during your lifetime? At the same time, your parents and sibilings have these very same ERV's in their genomes. Did your parents and siblings also suffer these same infections, and did those same infections result in identical insertions at identical positions in their genomes?
I know not all immunity is aquired. What I am saying is that your ghosts and so called remnants could be saying nothing at all as far as ancestry to apes is concerned. The few inconsistencies and contradictions mentioned this far appears to consolidate and support my assertion.
Not only is ther HGT but there is also epigenetic inheritance going on, as well as changes throught a sinlge lifetime. I don't think your researchers truly have any clue how to differentiate what's what and when it got there other than by applying evolutionary assumptions.
Let's not move on untill you
1. Can explain why PTERV-1 is not found at an ancestral point in humans and orangs?
2. Why guinea pigs have the same ERV in the same genomic region as humans?
3. How can researchers tell if an ERV has been transmited via HGT, epigentic inheritance etc, as opposed to ancestry?
If you cannot answer these, then I guess the whole point to where you are going with this is mute.
If you cannot explain the inconsistencies and contradictions to a theory then effectively what you call evidence for common ancestry via ERV's is no more robust than quoting from the Bible.
Edited by Mazzy, : No reason given.

This message is a reply to:
 Message 983 by Taq, posted 07-27-2011 2:49 PM Taq has replied

Replies to this message:
 Message 990 by Taq, posted 07-27-2011 7:04 PM Mazzy has not replied
 Message 992 by Nuggin, posted 07-27-2011 7:07 PM Mazzy has replied
 Message 996 by ZenMonkey, posted 07-27-2011 10:46 PM Mazzy has replied

Mazzy 
Suspended Member (Idle past 4590 days)
Posts: 212
From: Rural NSW, Australia
Joined: 06-09-2011


Message 988 of 1075 (626210)
07-27-2011 6:36 PM
Reply to: Message 985 by Taq
07-27-2011 4:07 PM


Re: Repeating the Topic
Taq says
In order for me to address this claim we first need to agree on the basics of retroviral insertion.
Above, I made a calculation for the probability of getting 10 orthologous insertions. Do you agree with these calculations or not?
No we don't. You need to explain why plain proof for no ancestry between chimps and humans gets convoluted into something it is not. What you need to do is explain why. I doubt that you can given your leading researchers are unable to do anymore than guess.
PTERV-1 was species specific and these infections occurred after the different lineages branched of of their common ancestors. The fact that retroviruses continue to infect species does not, in any way, refute the fact that orthologous ERV's are inherited from a common ancestor. If humans do not share a common ancestor with other apes then you should not find a single orthologous ERV, but instead you find tons of them.
You might as well try to refute the argument that French and Spanish share a common ancestral Latin language by pointing to the differences between the languages, forgetting that it is the commonalities that point to their common ancestral language.
Also, the pages you linked to talked about the GULO pseudogene. This is not an ERV.
I am not saying that aquisition via HGT disproves anything. What I am plainly stating is that these annomolies and nconsistencies open the back door to other possibilities therefore rendering ERV's useless in identifying common descent. It is bad enough to suggest we evolved from apes, let alone show a similar connection to a guinea pig.

This message is a reply to:
 Message 985 by Taq, posted 07-27-2011 4:07 PM Taq has replied

Replies to this message:
 Message 989 by Nuggin, posted 07-27-2011 7:02 PM Mazzy has not replied
 Message 991 by Taq, posted 07-27-2011 7:06 PM Mazzy has replied

Nuggin
Member (Idle past 2492 days)
Posts: 2965
From: Los Angeles, CA USA
Joined: 08-09-2005


Message 989 of 1075 (626217)
07-27-2011 7:02 PM
Reply to: Message 988 by Mazzy
07-27-2011 6:36 PM


Re: Repeating the Topic
You need to explain why plain proof for no ancestry between chimps and humans gets convoluted into something it is not.
Not to trip the triple negative but...
We don't need to explain why plain proof of no ancestry is anything, since there is no proof of no ancestry.
Or written another way:
We don't need to disprove you lack of evidence to support you assertion that something didn't occur.

This message is a reply to:
 Message 988 by Mazzy, posted 07-27-2011 6:36 PM Mazzy has not replied

Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(2)
Message 990 of 1075 (626219)
07-27-2011 7:04 PM
Reply to: Message 987 by Mazzy
07-27-2011 6:23 PM


Re: Moderator Advisory
If we are talking about PTERV-1, it was not found in the right spot in humans nor orangs so these calculations do not apply to how amazing it was for PTERV-1 to reside in a particular exact spot of the human and chimp genome.
PTERV-1 insertions are NOT found at the same spot in human and chimps genomes, or any genome for that matter. That's the whole point. They are non-orthologous. Not one PTERV-1 insertion was unambiguously found at the same same base in any of the genomes. The PTERV-1 insertions in the chimp and gorilla genomes were NOT found at the same bases.
So again, what is wrong with the calculations? Those calculations are for predicting how many insertions it takes before two occur at the same position.
They can construct their models to pick up what they want, the point is they did not pick up PTERV-1 in the human and orang where it should be if it was inhereted, thereby falsifying the validity of any ancestral connection between chimps and humans.
No one is saying that PTERV-1 insertions were inherited from a common ancestor. They were inserted after each lineage branched off from the common ancestor. That is why they are NOT found at the same location in each genome.
Can you please explain how acquiring non-orthologous ERV's after splitting from the common ancestor invalidates orthologous ERV's as evidence of that common ancestor?
As for how this retroviral infection bypassed orangutans and humans, the authors offer a number of possible scenarios. Whatever conclusions that are made of this are based on predetermined assumptions of what is related to what and this becomes a part of the insertion values in any model.
No predetermined models. In order to determine which lineages were infected by PTERV-1 they looked for the lineages that had PTERV-1 inserts. That's it.
WOW!...Integration site preferences as I mentioned...Go figure!
How many sites are there? How many bases in the genome are found in these integration sites?
From the paper I quoted earlier for HIV integration site preferences:
quote:
For HIV the frequency of integration in transcription units ranged from 75% to 80%, while the frequency for MLV was 61% and for ASLV was 57%. For comparison, about 45% of the human genome is composed of transcription units (using the Acembly gene definition).
Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences | PLOS Biology
45% of the human genome is about 1.5 BILLION bases. The chances of a HIV virus inserting into the same base twice is 1 in 1.5 billion. The odds of winning the Powerball lottery are better than that, and yet you think it happens with ease. Care to explain?
What I am saying is that your ghosts and so called remnants could be saying nothing at all as far as ancestry to apes is concerned.
All this time you have been arguing that they are retroviral insertions, and now you are saying that they are not? You should really make up your mind.
The fact remains that you and your siblings (assuming you have siblings) share the same ERV's at the same location in your genomes because you inherited them from your parents which are the common ancestor of you and your siblings. It is not due to being infected by the same virus 200,000 times and having those viruses insert at the same location in each genome.
With that said, if one of your siblings acquired a new ERV through a new infection would the presence of that new ERV negate the evidence of common ancestry seen in the ERV's you do share? If your sister gets infected by a retrovirus are you no longer sisters?
1. Can explain why PTERV-1 is not found at an ancestral point in humans and orangs?
Because PTERV-1 did not infect the common ancestor of humans and orangutans. It infected a select few apes species after each lineage had split from the common ancestor of those lineages. It is the same as your sister acquiring a new ERV after you are both born. That is why the ERV is found in your sister and not in you while the orthologous ERV's you inherited from your parents are still there for everyone to see.
2. Why guinea pigs have the same ERV in the same genomic region as humans?
GULO is not an ERV, it is a pseudogene.
3. How can researchers tell if an ERV has been transmited via HGT, epigentic inheritance etc, as opposed to ancestry?
They can tell by the base they are inserted into. ERV's found at the same base (i.e. orthologous) in two or more species are due to a single insertion in a common ancestor. ERV's that infect the lineage after they have split from the common ancestor are not found at the same base (i.e. non-orthologous).
If humans and other apes do not share a common ancestor then you should only find non-orthologous ERV's. You don't. You find orthologous ERV's as well as non-orthologous ERV's.
Also, epigenetic inheritance has nothing to do with DNA sequence. Epigenetic inheritance has to do with DNA methylation and histone packaging. We are talking about sequence data, so epigenetics is not a factor.
Edited by Taq, : No reason given.

This message is a reply to:
 Message 987 by Mazzy, posted 07-27-2011 6:23 PM Mazzy has not replied

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