Rickets and arthritis are not evidence of being human. Kittens can get rickets; dogs can get arthritis. Also, Rudolf Virchow died in 1902. He was not (for example) able to do a genetic comparison. He also thought that the flattened skull was due to a powerful blow to the head. It seems that most of his theories about neanderthals have been disproved by further discoveries.
Erik Trinkaus also thinks that neanderthals are not human. So, despite your quote suggesting that neanderthals are fully human, the person you quoted does not think they are.
I think Neanderthal may be Nephilim. There were plenty of them so why not expect to find some fossil evidence for them.
I believe what you have found is DNA evidence of a human foxp2 gene and a 99.5% similarity to modern humans which is in the usual human variation range. There is still inconclusive proof as to whether or not mating accured at all, the latest being none or little interbreeding.
Now we are talking around about 30,000 years ago and the findings cannot clarify this with certaintly. Let me point out that the very evidence I use from your researchers to support my points is the same research I believe has no validity. I have spoken to my thoughts on algorithms, assumptions and probabilities. If your research is unable to provide definitive proof of whether or not mankind bred with Neanderthal what hope has it got of best guessing accurately anything past that time? Anyway, I will refer to your evolutionary research.
Neanderthal supposedly has the human variation of the FOXp2 gene. Now we all know that is not all there is to language and intelligence. Genes work in families. However, based on this being an accurate assumption and the models have best guessed and assumed correctly then Neanderthal has this FOXp2 gene. He is human, but something is still very different about him. Neanderthal could have become this way due to environmental factors and deviated from an already modern human look and simply be a human. Neanderthals appearance in the record, genetic differences, physicall differences and strength, and sudden demise can be explained by Nephalim and flood.
Because of the huge variation and homology between species anyway, and not knowing what the initial ape kind looked like, using morphology alone is problematic. The human variation of the Foxp2, for the moment and depending on the veracity of any of these comparisons, Neanderthal appears to be perfectly human.
Turkan boy with his small (compared to modern humans) thoracic spinal canal diameter, was unlikely to have sophisticated speech. I support this further with side views of the skull showing his ape face as being unable to speak and hold conversations also.
It does not matter what these researchers used to think. The point is that now even your own researchers put Neanderthal along side Homo Sapiens in physical and genomic comparisons.
Now to bring this back to the topic base of homo erectus and its classifications. The side view of Turkana Boys skull shown in the link below clearly demonstrates this best example you have of an erectus ape becoming human but looks nothing like a human of any race. It is nothing like Neanderthal or mankind. It does not matter how much you highlight less of this or that, it simply does not look anything like a human. The picture also demonstrates Turkana Boy is similar to other reconstructions and fossils of other non human primates.
We do not have DNA from erectus, so morphology has to do. To me the morphology of Neanderthal is well within human range today as always and your researchers are saying he is human. I am happy to accept him as human based on your data, for now.
Homo Erectus is not anywhere near looking human, regardless of the similarities of this and that, the front view of the skeleton, or arms or bipedalism or anything else. This along with flat faces being around for over 12my in primates anyway, like Lluc, means Homo Erectus is more like an ape than a human or Neanderthal by far.
I may not have a robust complicated classification system, but regardless this appears clear to me. It is a matter of interpretation of the information at hand. You have theories as to why intermediates did not survive and I say there never were any because your intermediates are apes.
First of all, if this claim of yours were true, then the ERV trees would NOT match the morphological trees or trees of descent.
You are claiming that the exposure to these viruses is essentially random. Then why do humans and chimps share MORE ERVs than humans and gorillas? Why do humans and gorillas share more than humans and baboons?
If what you were claiming were true (and I think you and I both know it's not) we'd expect roughly the same number of ERVS to be shared by humans and chimps as ERVs shared by gorillas and humans with no correlation between the three.
That's NOT the case.
Further, you have REPEATED your false claim that these things are inserted in "similar" places. Not similar. The SAME.
The genome is EXTREMELY long. The odds of two independent organisms being exposed to the EXACT SAME STRAIN of the EXACT SAME VIRUS and having it show up in the hereditary genome in the EXACT SAME PLACE are ASTRONOMICAL. And that's for ONE ERV. We're talking MANY MANY MANY ERVs.
I know you are a big proponent of "Jesus Magic" as far as answers go, but unless you can demonstrate that this magic is being used to work out virus position, your claim holds no water whatsoever.
Nuggin, I am not sure if ERV's fits in with the topic parameter set by admin.
If it is OK to go there I will provide a more robust refute.
I will make these comments until then ..Read the papers I put up which will better clarify whom exactly believes in magic.
I will say if ERV's in every species demonstrates a dilineation of ancestral lineage then predictively the not finding of same would disprove the connection. You have found such ERV's not present in humans and only present in non humans. Therefore the basis for the theory is falsified and you need to get some more theories in to save the whole concept. That is how I see it.
Therefore, it appears, ERV's are not a reliable nor predictive method in themselves to difinitively speak to ancestry.
Let's not forget it was not that long ago reseachers considered non coding DNA junk as spoken to in the link below, and what you actually find as evidence are ghosts and remnants based on complicated models that have many confounding variables and assumptions within.. http://www.sciencedaily.com/...ases/2002/08/020802075138.htm
And really researchers are not clear on what they are looking at...
"Our analyses indicated that the HERV-F LTRs and HERV-K (C4) LTRs have the same degree of divergence, indicating that these HERVs were integrated at about the same time. This calculation contradicts the interpretation of the Southern blot analysis, as this indicates that the HERV-Fs were integrated before the split between the New World and Old World primates. However, it should be remembered that there is an inevitable degree of uncertainty when calculating rates of divergence, particularly over such short genetic regions, and that there are no guarantees of equal mutational rates in the different HERV elements. There is of course also the possibility of cross-hybridization between conserved pol regions of different retrovirus origin in Southern blot analysis" http://vir.sgmjournals.org/content/80/9/2383.full
Since your reply is completely unconnected to my post, I am left thinking that you simply love the 'sound of your own voice' and will therefore post reams of text while showing little interest in other people's posts. You have apparently failed to change your modus operandi. Good luck with that.
I disagree. You appeared confused as to whether or not you were supporting Neanderthal as being human, not human, or in the middle somewhere.
I thought my post, with appropriate links, clarified the point that Neanderthal is human, which is what I am asserting. Nothing more or less. Being Nephalim means he is still human as angels bred with humans and not apes, as far as I know anyway.
It appears to be evolutionists that are having difficulty explaining why Neanderthal is classed as a different species to Homo Sapiens given current research and comparative similarities. However the recent research only backs up Neanderthal being more human than he ever was, that is if it is valid research. So you and I should have no problems with Neanderthal.
You do not clarify it's separation from Sapiens yourself yet you accuse me of not responding appropriately.
Sometimes we dance on the same page on a couple of things, so I do not understand what further clarity you require from me, while staying within topic guidelines set out. Perhaps you just want to disagree for the sake of it.
Feel free to clarify with me exactly what it is you are requesting clarification of re Nenaderthal if you feel it is appropriate to the thread and furthering the discussion!
Nice double standard you have there. That 99.5% similarity was a result of single base pair comparisons, not the 30 base pair comparisons that you use to say that chimps and humans are 30% different.
Again I ask, what is this all about? Are you disagreeing with your own researchers in saying Neanderthal is perfectly human? Are you disagreeing that the holistic comparison is 30%, if not, then I would suggest that by your own research chimps are not as similar to us as once thought. No matter if any comparison was 2%, 30% or 80% difference it would all 'prove' evolution. Is that what you are suggesting?
I am more to the point suggesting it is your researchers that provide biased misrepresetations of DNA comparisons. Right fromn the start when they first came up with the 98% hit I'd say a reasonabe creationists prediction may have been that this is ridiculous given the difference between man and beast. With further research a more holistic comparison has been done that cites 30%. It is more a matter of picking and choosing to focus on the one genomic region that will provide such high comparisons rather that viewing the genome holistically.
The same goes for junk DNA that creationists have always asserted cannot be junk DNA have now been vindicated in that junk DNA is very important.
Look at this article
"PTERV1 contains three structural genes -- gag, pol, and env -- and regulatory sequences called long terminal repeats (LTRs). To further explore the evolutionary history of the retroviral elements, the authors compared the sequences of gag and pol, as well as the LTR sequences, for each infected primate species. The sequence history, they discovered, did not comport with the established evolutionary history of the primates themselves. Divergence between macaque and baboon was significantly greater than between gorilla and chimp -- even though slightly more evolutionary time separates gorilla and chimp than macaque and baboon." http://www.sciencedaily.com/...ases/2005/03/050328174826.htm
Did not comport with established primate history means to me that you may pick and choose what you use as evidence and disregard anything that is uncomfortable, and propose more theories to explain the unpredicted and contradictory.
ERV's do not prove to me that there is an ancestral connection to apes. Neither is the fossil evidence convincing and really I do not know what else I can say. If it is not observed it is theoretical. If it is theoretical it is a matter of faith. Theories have theories and assumptions to back them. My assumptions are different to yours but not necessarily wrong.
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." http://www.plosbiology.org/...10.1371%2Fjournal.pbio.0030110
So Taq, would you like to repost or shall I try to reply seriously to this post of yours.
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.
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:
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.
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.
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."
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.
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." .....
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.
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.
So what is wrong with the calculation? For HIV, there are about 1.5 billion bases amongst all of the insertion sites that it can insert into. Therefore, the odds of an HIV virus inserting into the same base in two different insertions is 1 in 1.5 billion, is it not?
It is not about the calculation it is about the fact that PTERV1 is NOT found at an ancestral site in the human and orang. No amount of number crunching is gong to put it there.
In fact if you want to crunch numbers you should take a look at this...
In this light it is interesting to note that over 30,000 different ERVs are known within human genome. 37,43 The range of the total human genome occupied by ERV sequences is anywhere from 1% to 8% - depending upon the reference (with more recent references favoring 8% or greater). The same range is true for the chimp genome as well.41 In fact, more recent work suggests a 45% ERV origin for the human genome at large (Mindell and Meyer 2001) and 50% for mammalian species in general ( Link ). In any case, of these tens of thousands of recognizable ERVs, only seven are currently known to infect both humans and chimps at identical locations within the separate genomes ( Link ). Isn't it interesting that out of 30,000 ERVs only 7 of them are known to have inserted at the same site in humans and chimps? - What are the odds given the known preference of many ERVs for fairly specific hot spot insertions? Yet, this is the argument for ERVs being evidence of common descent as per Talk.Origins: http://www.detectingdesign.com/pseudogenes.html
If you want to crunch numbers cruch out how many tens of thousands of ERV's there are, how may sites are regarded as ancestral sites and the probability of infection due to random chance, statistically of infecting such sites.
Only 7 or so of hundreds of thousands have actually been shown to do so. I would hardly call this convincing.
Evos go on and on about testable theories supported by validation and observation. ERV's as a method of demonstrating ancestry has exceptions, inconsistency and contradictions.
How are these anomolies validating this ERV theory by evidence and observation? They do not. It is falsified on more than one basis.
If something is falsified you can crunch numbers all you like, and I can agree all I like, and they still will mean nothing more than wishful thinking.
1. Can explain why PTERV-1 is not found at an ancestral point in humans and orangs?
Because the human orang line split before the human chimp line
If my friends gave me this reply I would know they were evading the question. If some I don't know gives such a simplistic reply they are either avoiding the question or do not know any better.
The question relates to why PTERV1 is not found in an ancestral point in humans in the same point it is in chimps?
2. Why guinea pigs have the same ERV in the same genomic region as humans?
Guinea pigs and humans are both mammals, an ERV in the same place in both would have been present in the ancestor mammal to both groups.
The number of ERVs shared between GPs and Humans is much less than those shared by closer ancestors.
This is also avoiding the point to the question. If guinea pigs and humans share a retrovirus then for this to show the ancestry of all mammals to humans it should be in all mammals It isn't.
"A retrovirus endogenous to guinea pig cells was earlier shown to be morphologically similar to type B and type D prototype retroviruses. Molecular hybridization techniques were used to show that guinea pig virus nucleotide sequences are endogenous to both domestic (Cavia porcellus) and indigenous (Cavia aperea) guinea pigs, but cannot be detected in the DNA of either other hystricomorph rodents or other mammals tested. " http://www.ncbi.nlm.nih.gov/pmc/articles/PMC288566/
3. How can researchers tell if an ERV has been transmited via HGT, epigentic inheritance etc, as opposed to ancestry?
Because it's present in the same place in ALL cells. That can only occur if the infection takes place at the SINGLE cell stage.
Could it happen ONCE that by happenstance a fertilized egg happened to get and ERV just before it split into 2? Sure. ONCE. Not hundreds of thousands of times.
This is also avoiding the question. Once a horizontally transmitted ERV reaches the germ line, which they sometimes do, how do you differentiate this ERV was transmitted horizontally rather than vertically if it is dated back past 1my or more. I say that you cannot differentiate.
In other words when you find this so called remnant of some virus in the so called same spot in a chimp and human, how can you tell that one was not horizontally tranfered, hit the germ line and ended up in the same spot as one verticaly inherited through preference of randomness?
You may have read this from the cited article
To summarize, evolutionists usually gloss over at least a few important facts when discussing the topic of ERVs. Many retroviruses can infect both humans and apes. The most notable of these is HIV, which is widely believed to have originated as SIV in chimpanzees, but can also infect humans, apes, and monkeys. It is entirely possible, therefore, that humans and apes were independently infected with the same virus given so many different ERVs and the similarity of the human and ape genomes.
Also, some retroviruses have been shown to have highly targeted insertion points, meaning that the virus selects very specific segments of the genome for insertion. Consequently, it is entirely possible that the same virus infected both humans and apes, and targeted the same location. This seems especially plausible in light of the fact that humans and apes have tens of thousands of endogenous retroviruses in their respective genomes. In other words, given so many thousands of different types of ERVs all targeting fairly specific locations, it is actually likely that at least a few of these retroviruses will infect both humans and apes at the very same location within the respective genomes without any need to invoke the common descent hypothesis.
To add to this, the theory that retroviral insertions are conclusive phylogenetic markers has been falsified by studies that have shown that, "Although independent insertions at the same locus may be rare [viral] insertions are not homoplasty-free phylogenetic markers".9 This would seem to be especially true given so many known ERV insertions that are at least generally targeted.
Additionally, some endogenous retroviruses are now known to be functionally indispensable - i.e., they are actually functionally beneficial and even vital to species' survival. If a particular retrovirus is functionally advantageous, that would only add to the plausibility of how a retrovirus can spread to the entire species without the need for common descent or dramatic population bottlenecks. It also presents the possibility that retroviruses were used as part of the original creative process; as retroviruses are often used in genetic engineering today, to introduce new genetic material to cells or aid in the transportation of genetic information (see Link - last accessed 3/10/09). " http://www.detectingdesign.com/pseudogenes.html
Once anhorizontally transmitted ERV hits the germ line it may well show its preference by ending up at the exact ame place in both species, anyway, and through vertical transmision. HGT in prokaryotes is much more common than initially thought.
Just ONCE I would love it if one of you Creationists held yourself to ANY SORT of standard.
You've failed to explain the inconsistancies in your claims for 1000 posts in this thread, yet here you are bitching about other people who ARE explaining.
No, actually what is astonishing is your trying to show how an ERV ends up in the 'right place' in two species while using an ERV that does not link humans and chimps as an example to demonstrate it.
What is even more astonishing is your inability to answer questions in more than a simplistic and misrepresentative way, after all the disparraging remarks you have aimed at me.
Unfortunately for you what we are discussing is not the creationist standards that you evos like to pick to pieces. At the moment it is about ERV's and their veracity in being used to establish common ancestry. This is not about a little inconsistency I am picking on here. This is about many inconsistencies and huge contradictions that totally falsify the entire concept.
I am saying, and have given many examples of where ERV's show inconsistent results that do not link close species together and rather link very distantly related species together.
If a theory is bolstered by the continual verification of data observed then your ERV's, as support, let alone proof, of common descent, is sadly lacking. Rather current data falsifies it time and time again.
Of tens of thousands of ERV's only about 7 have been shown to demonstrate this magic in humans Have you crunched the numbers yet to see the statistical inherant possibility that of all these EVR's a few of these retroviruses will infect both humans and apes at the very same location within the respective genomes without any need to invoke the common descent hypothesis?
I'd say the answer will be around 7.
So you have avoided the strong points within my questions. For an evolutionist of your calibre and apparent knowledge it is inexcuseable.
Why on earth would evolutionists claim this is good evidence for common descent? I have cited near as many examples of this all being nonsense as your reserchers have actual examples of this occuring.
For you to continue to use ERV's to demonstrate mankind must have had ancestors leading back to an ape you must have much faith because you do not have science behind it.
In actual facts my 1000 posts have made an ape out of your Homo Erectus and put the rise of humanity from apes into the realm of faith. I have also shown that ERV's as a support for common descent has been falsified and is only kept alive by the plethora of excuses and theories made up to address the contradictions.
So the remaining question to give a simplistic answer to is "Why are ERV's used to show common descent re humans and apes when there are more examples that falsify it available then there is actual evidence for it?"
Please explain, if you are going to pusue ERV's in this discussion.
You can rule out horizontal gene transfer as a possible route for ERVs to make their way from chimp to human, or from any primate to another, which is what you seem to be implying. As far as I know, HGT almost always happens between single cell organisms, very rarely between multi-cellular organisms, and never between vertebrates.
Note that word, never.
The let me state very simply that you are very wrong.
Mazzy, I'm trying very hard to pretend you aren't intentionally being dishonest.
But then you come along and make a claim like ther eare "only 7 of them which are shared between chimps and humans".
EVEN YOU know that that's bullsh1t.
When you deliberately *** in a fashion where you can't help but get caught it just shows us that you have absolutely no intention to argue in good faith. It shows us that you KNOW you are wrong but are just arguing because "Jesus loves ***".
You need to stop.
I think you need to stop making baseless accusations. If there are more then name them. The article said 7. It doesn't matter if it is out. The person that wrote the article is a science head and likely knows as much as you guys.
It is not about just the number of ERV's idenitifed to promote ancestry with chimps. It is about the fact that Horizontal Gene transfer as well as epigentic inheritance are other forms of non-vertical transmission of genes. This opens the doors to non verticle inheritance of ERV's and their 'ghost relics' being found n certain places within the genome.
You do not have to believe little creationist me. This is from your body of research. The fact that you may be totally ignorant of it is not my responsibility.
Not only can HGT and epigenetic information reach the germ line, some ERV's have been found to actually be required and functional. With time you are going to see more and more of this as has been the case since the articles above were written.
Here is another article you may find interesting:
The Perils of Dogma
"IT WILL TAKE YEARS, perhaps decades, to construct a detailed theory that explains how DNA, RNA and the epigenetic machinery all fit into an interlocking, self-regulating system. But there is no longer any doubt that a new theory is needed to replace the central dogma that has been the foundation of molecular genetics and biotechnology since the 1950s.
The central dogma, as usually stated, is quite simple: DNA makes RNA, RNA makes protein, and proteins do almost all the real work of biology. The idea is that information is stored in the twisted ladders of DNA, specifically in the chemical bases (commonly labeled A, T, G and C) that pair up to form the rungs of the ladders. A gene is just a particular sequence of bases on one side of the ladder that specifies a protein." http://www.mindfully.org/GE/2003/Junk-GenomeNov03.htm
Here is a bit more...
"In the past, mathematical models of evolution have focused largely on how populations respond to single mutations, the random changes in single nucleotides on the DNA chain. Other theories have focused on recombination, the process that occurs in sexual selection when the genetic sequences of parents are recombined.
The new mathematical model, developed by Rice's Michael Deem and visiting professor Jeong-Man Park, attempts to find out how HGT changes the overall dynamics of evolution. In comparison to existing models that account for only point mutations or sexual recombination, Deem and Park's model shows how HGT increases the rate of evolution by propagating favorable mutations across populations" http://www.scienceagogo.com/...029220033data_trunc_sys.shtml
This article I believe won an award. At the moment your researchers are scurrying to invent models that are meant to address these confounding variables. Good luck to them.
So it appears it is OK for Taq to swear at me and you to baselessly call me a fibber. You had best stop and try to mount some decent refute.
The point I have made is that there is more than enough contradictions eg ERV's connecting humans to guinea pigs whilst not all mammals, ERVs not in humans but in other primates. tens of thousands of ERVs with few that are actually examples and many that are contradictions. This along with the possibility of HGT and ERV preferences opens the door to other ways in which ERV's can end up where they are, is more than sufficient evidence for skepticism.
Additionally much of these results involve population sizes and bottlenecks. Your researchers have no idea of population size. It is based on probabilities etc. Rather they make the population size fit their model to arrive at the result they require. As for population bottlenecks they are basically fluff. TOBA and KT have much the same representation of species after the event as prior to the catastrophe. If you want links for verification because you are not up to date with the latest research just say so and request and I will provide plenty to amend any ignorance.
All you evos pay out on creationists when we have a dig at your theory. You say your theories are backed by results that support the theory and that makes it reliable and as good as factual. Well, here is the big news. Much of data is contradictory. It is sufficiently contradictory that is is now not reliable. It has not continued to be supported and as far as I, and many other creationists believe, it has been falsified.
There are no levels of falsification as just one example is sufficient to falsify any theory. There is no just a little falsified, a theory either works all the time or it does not. The fact that you continue to 'mend' your initial bases with more and more theoretical assumptions is hardly a faith changing paradigm. In fact the more a creationist learns and delves into your research, the less ignorant they are of it, all the more reasons are found for skepticism.
So basically I maintain that ERV's are not a reliable, consistent determinor of common ancestry anymore, if they ever were. It is a matter of faith that you continue to regard them as a valid.
I am not trying to disprove evolution. It is based on theory and assumptions as are my and any other creationists propositions. I am suggesting that there is more than one hypothesis that runs along side the theories you have re intermedites extinction.
It turns out that the Guinea pig also shares a non-functioning GULO gene with a few of the same deletions found in the primate GULO gene. Although there are some differences noted as well, the similarities in the deletion areas raises some serious questions about the assumptions underlying the entire pseudo-gene argument for evolution. (see below diagram). 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.
There is no point in my providing links if you are not going to read them. You should be aware of the contradictions regarding ERV's without my having to spoon feed them to you.
And . . ?
...and they are not found in all mammals. Hence a contradiction to the simplistic response you provided.
The loss of activity of the gene for L-gulonolactone oxidase (GULO) has occurred separately in the history of several species. The loss of this enzyme activity is responsible for the inability of guinea pigs to enzymatically synthesize vitamin C, but this event happened independently of the loss in the haplorrhini suborder of primates, including humans. The remains of this non-functional gene with many mutations is, however, still present in the genome of the guinea pigs and in humans. The function of GULO appears to have been lost several times, and possibly re-acquired, in several lines of passerine birds, where ability to make vitamin C varies from species to species. In addition, GULO activity has also been lost in all types of bats, regardless of diet.
Loss of GULO activity in the primate order occurred about 63 million years ago, at about the time it split into the suborders haplorrhini (which lost the enzyme activity) and the more primitive strepsirrhini (which retained it). The haplorrhini ("simple nosed") primates, which cannot make vitamin C enzymatically, include the tarsiers and the simians (apes, monkeys and humans). The suborder strepsirrhini (bent or wet-nosed prosimians), which are still able to make vitamin C enzymatically, include lorises, galagos, pottos, and, to some extent, lemurs. http://en.wikipedia.org/wiki/L-gulonolactone_oxidase
ERV's transmitted horizontally are non-orthologous. ERV's transmitted vertically are orthologous. I have said this multiple times now
Is that so? Well then you had best spek to this reseach that disagrees with you.
"Retroviruses normally infect the somatic cells of their host and are transmitted horizontally, i.e., in an exogenous way. Occasionally, however, some retroviruses can also infect and integrate into the genome of germ cells, which may allow for their vertical inheritance and fixation in a given species; a process known as endogenization. Lentiviruses, a group of mammalian retroviruses that includes HIV, are known to infect primates, ruminants, horses, and cats. Unlike many other retroviruses, these viruses have not been demonstrably successful at germline infiltration. Here, we report on the discovery of endogenous lentiviral insertions in seven species of Malagasy lemurs from two different genera—Cheirogaleus and Microcebus. Combining molecular clock analyses and cross-species screening of orthologous insertions, we show that the presence of this endogenous lentivirus in six species of Microcebus is the result of one endogenization event that occurred about 4.2 million years ago. In addition, we demonstrate that this lentivirus independently infiltrated the germline of Cheirogaleus and that the two endogenization events occurred quasi-simultaneously." http://www.plosgenetics.org/...0.1371%2Fjournal.pgen.1000425
Now I have demonstrated multiple times that you are wrong.
No, it won't. There are billions of hotspots. The chances of two viruses inserting into the same hot spot is 1 in 1.5 billion for HIV. Remember those calculations you keep ignoring? This is where they come in.
Remember my request to cruch numbers for the tens of thousand of ERVs present in the human genome that could end up in certain places due to site preferences and randomness, not to mention them being there due to horizontal gene transfer or epigentic inheritance. I have provided the information for you to ignore.
"In this light it is interesting to note that over 30,000 different ERVs are known within human genome. 37,43 The range of the total human genome occupied by ERV sequences is anywhere from 1% to 8% - depending upon the reference (with more recent references favoring 8% or greater). The same range is true for the chimp genome as well.41 In fact, more recent work suggests a 45% ERV origin for the human genome at large (Mindell and Meyer 2001) and 50% for mammalian species in general ( Link ). In any case, of these tens of thousands of recognizable ERVs, only seven are currently known to infect both humans and chimps at identical locations within the separate genomes ( Link ). Isn't it interesting that out of 30,000 ERVs only 7 of them are known to have inserted at the same site in humans and chimps? - What are the odds given the known preference of many ERVs for fairly specific hot spot insertions? "
"Although retrovirus integration can occur throughout the genome, local "hot spots" for integration exist where a strong preference for particular sites over others can be demonstrated statistically. Recent work with HIV and murine leukemia virus has implied that there is also a preference for integration into transcribed regions of the host genome, in the case of murine leukemia virus, near transcriptional start sites. The basis for these preferences is unknown, but they may reflect interaction of the pre-integration complex with specific proteins or with specific DNA sequences or structures that are associated with transcription." http://www.pnas.org/content/102/5/1436.full http://www.detectingdesign.com/pseudogenes.html
The real number is around 200,000, not 7. Only a few hundred ERV's are non-orthologous between chimps and humans. Over 200,000 are orthologous. Links can be found in my post above.
I missed it, but will have a look. It doesn't matter even if you are correct. The point being it takes just one to thwart and falsify theory and HERV-K is one. It also makes a mess of your primate phylogeny and separates humans from chimps.
You haven't cited one yet
PTERV1 insertions do not falsify common descent because they are non-orthologous. I have said this time after time and you refuse to deal with it. If PTERV1 insertions were orthologous then that would falsify the ERV evidence, but they aren't.
And what did it take to say it was orthologous....dating, rather than looking for and recognizing ghosts.
"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely (Figure S3). . .
Several lines of evidence indicate that chimpanzee and gorilla PTERV1 copies arose from an exogenous source. First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon, making it unlikely that endogenous copies existed in a common ancestor and then became subsequently deleted in the human lineage and orangutan lineage. Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect, as has been proposed by a minority of anthropologists." [emphasis added] 42
"Inconsistencies do exist with phylogenetic analyses and are often explained by ad hoc arguments without positive evidence." ( Link - last accessed 3/10/09)
Not even precambrian humans are going to falsify your theory according to you.
Endogenous retroviruses may arise within genomes by at least two different mechanisms: retrotransposition from a pre-existing endogenous retrovirus (intraspecific transmission) or infection and integration via an exogenous source virus (horizontal transmission). Many cross-species transmissions have been documented and frequently manifest themselves as inconsistencies in the presumed phylogeny of closely related species. During the 1970s and 1980s, Benveniste and colleagues identified, by DNA hybridization and immunological cross-reactivity, several retroviral elements that could be found among more diverse primate/mammalian species but not necessarily among more closely related sister taxa [12,13,14]. *** and colleagues, for example, reported the isolation of a particular class of type C retroviruses from a woolly monkey (SSV-SSAV) and gibbon ape (GALV) but not the African great apes . These viruses shared antigenic properties with previously described type C activated endogenous retroviruses of the Asian feral mouse Mus caroli. Cross-species infection from murines to primates was proposed as the likely origin of the retrovirus. A related endogenous retrovirus was subsequently identified in the koala, suggesting a zoonotic transmission from placentals to mammals . Evidence of horizontal transmission for other families of retrovirus has been reported among classes of species as distantly related as avians and mammals http://www.plosbiology.org/...10.1371%2Fjournal.pbio.0030110
PTERV1 remains a virus that is not found in Humans and Orangs. It is theorised to be non orthologous because when these researhcers went looking for it, PTERV1 had disappeared from the human genome and a stack of convolutions are required to explain it as always. The excuse is HGT.
The major point being, just one example of inconsistency is suffient and info re HERV-K is one and makes a mochery of the entire concept. I need no more that this to allege the inconsistency and unreliability of these ERV's as support for common descent.