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Another poor response to ERV evidence for common ancestry by a creationist.

Loudmouth

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Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences (PLOS Biology)


I thought there is more and more research that suggests ERV elements are not inserted randomly.

As MG describes so eloquently in his posts, the target site preferences are for larger genomic features. Insertion is still random with respect to locus. From that paper:

"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)."
PLoS Biology: Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

HIV preferrentially inserts into transcription units, or areas of the chromosome that are not wrapped up in histones and are being actively transcribed (if I am understanding the paper correctly). These sites make up 45%, or about 1.5 billion bases, of the genome. Within these areas, HIV inserts randomly with respect to the base sequence.

Another reference that MG references looked at ~40,000 insertions and only found 41 that inserted into the same base. Using this number as an upper limit, of the 200,000 ERV's found in the human genome we should only find 0.1% at the same places in the chimp genome, or 200 orthologous ERV's. Instead, we only find ~200 that are NOT orthologous, the exact opposite of what we should find if humans and chimps do not share a common ancestor.

How do you tell a LTR has a viral base as opposed to being a functional element that only appears similar to a viral element?

For full length ERV's it is pretty easy. You find viral genes in between the LTR's. Since these repeats share strong homology it is possible for recombination to occur between the LTR's and "loop out" the viral genes, resulting in a solo LTR. So we have a known source for LTR's, and a known mechanism to produce solo LTR's from full length ERV's.

To use an analogy, how could a crime scene investigator tell the difference between a real fingerprint from one that was perfectly planted by the CIA? Well, he probably couldn't. However, I see no reason to free everyone from prison who was convicted through fingerprint evidence. The same goes for rejecting the ERV evidence.
 
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Greg1234

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Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences (PLOS Biology)


I thought there is more and more research that suggests ERV elements are not inserted randomly.
How do you tell a LTR has a viral base as opposed to being a functional element that only appears similar to a viral element?
:thumbsup: They are functional ScienceDirect - Gene : Endogenous retrovirus long terminal repeats as ready-to-use mobile promoters: The case of primate β3GAL-T5 I'm just trying to get it through to Mr Loudmouth.

Maybe what these researchers are seeing are not viral anythings. Is that at all possible?


It's based on Darwinian presupposition. DNA has viral like elements and these things that we call viruses are challenged by some to simply be dead genetic material (as seen in the link I showed you earlier). "That indeed, so-called viruses do not eat or drink, have no metabolism with which to change anything or generate energy, no secretions, no defecation, no activities, no nerves, sensors or (electrical) nerve energy, no reproductive faculties nor, in fact, any qualities of life whatsoever. Thusly, what are called viruses are indeed dead organic matter consisting of genetic and chromosomal RNA and DNA encased in a protein capsid, those capsids being identical to the capsids of the genomes within the many thousands of life units called mitochondria or organelles that populate every human cell from a few hundred up to 30,000 or more."

The invasion of the cell by the viruses is argued to simply be the process by which the cells eat this genetic material "That lifeless genomes do not and cannot invade cells as reported and photographed. What has been photographed are cells conducting eating processes called pinocytosis or phagocytosis wherein they absorb for recycling breakdown debris from disintegrated neighboring cells that have expired." And when it is broken down and recycled, some of the material is reused.

ERV elements inserting indiscriminately at random points within genetic material is a form of random mutation, although, on a larger scale. To interfere with genetic material the way random insertions would do, is highly detrimental. But this goes back to the idea that Darwinian mechanisms are viable, and that random integration, like random mutations, is simply another walk in the park.
 
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Loudmouth

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You do realize that this is the exact function LTR's have as part of the viral geome, don't you? The LTR's function as promoters for the viral genome.

It's based on Darwinian presupposition.

It is the same presupposition that a forensic scientists uses to connect a defendant to a fingerprint at a crime scene.

The invasion of the cell by the viruses is argued to simply be the process by which the cells eat this genetic material

Do you even understand how retroviruses work? Insertion into the host genome is part of the viral cycle. Insertion is followed by upregulation of the viral genome through the LTR promoters in order to produce more viral particles.

ERV elements inserting indiscriminately at random points within genetic material is a form of random mutation, although, on a larger scale. To interfere with genetic material the way random insertions would do, is highly detrimental.

Every time? I would like to see any references you have which demonstrate that random mutations are detrimental each and every time.

But this goes back to the idea that Darwinian mechanisms are viable, and that random integration, like random mutations, is simply another walk in the park.

We OBSERVE that retroviruses insert randomly, with respect to locus, into the host genome. Are you saying that you are rejecting the facts?
 
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We OBSERVE that retroviruses insert randomly, with respect to locus, into the host genome. Are you saying that you are rejecting the facts?
He's PRESUPPOSING that it can't happen that way and so it doesn't.

Define "irony" and you'll find a picture of a Christian trying to disprove evolution.
 
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Greg1234

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You have the cart before the horse. If what you say is true, then physiology is defined by the ERV's, not the other way around.

And physiological requirements dictate which ERV elements are needed to perform the task. The cart and the horse are at the same position.
What you are arguing for is diversification of species through ERV insertion which fits just fine in our argument.
No I'm not. You are.

It may conflict with the observed mutation rate of most LTR's, but it fits fine with common ancestry and subsequent evolution from that common ancestor.
This was geared toward the random integration argument.



So what functions are people missing if they don't have those 8 HERV's?
Irrelevant.


This doesn't explain it at all. The divergence of LTR's is within a single ERV and a single species. When retroviruses insert the LTR's (the bookends of the viral genome) are identical. If common ancestry is true, then the longer an ERV is in a lineage the more differences we should see between those two bookends within the same ERV. Look for an orthologous ERV shared by all apes, including humans, that still has both LTR's (the 5' and 3' LTR's). Next, find the sequence for the human version of this gene. Compare the differences between the 5' and 3' LTR's. Do the same for a human ERV that is only seen in humans and chimps. This comparison is only for human ERV's. What you will find is that there is more divergence in the LTR's of human ERV's that are shared by all apes than in the human LTR's of human ERV's shared by just humans and chimps.

How do you explain this?

I'll simplify it this time. Maybe you can get it. \

You say: LTRs in different organisms are different. But they were all identical upon insertion within some common ancestor. When the common ancestor mutated, thats how the differences arose.

I say: They were never identical. LTRs are different based either on function and/or minor mutation. Different organisms have different physiological requirements hence LTRs are different.

You say: Humans and other humans and humans and chimps share a higher degree of LTR similarity between them because divergence between humans is low.

I say: Humans share a high degree of LTR similarity because they have a high degree of functional similarities.

You say: There is more divergence in the LTR's of human ERV's that are shared by all apes

I say: LTRs which are shared by all apes cover a more physiologically diverse ground and hence would be less similar to each other.

We reuse parts and designs because we have limited time and resources. God has neither limitation. Therefore, there is no expectation of a nested hierarchy where creationism is concerned, correct?

No, irrelevant. Also, nested heirarchy was already addressed.

No, it was swept under the rug, as usual.
No it wasn't.

Does this adaptation require mutations? Or are you talking about phenotype plasticity? Peer review references?
This was just given.
 
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Loudmouth

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[qs]And physiological requirements dictate which ERV elements are needed to perform the task[/qs]

Sharpshooter fallacy. If we had different ERV's we would have different physiological requirements. There is nothing that requires humans as the end result, nor chimps, gorillas, bonobos, or orangutans. ERV's, if functional, produce variation, and natural selection works on that variation.

[qs]No I'm not. You are.[/qs]

That is exactly what your functional ERV argument is leading to, that they are required for species diversification. However, it does nothing to disprove ERV's as markers for common ancestry.

[qs]Irrelevant.[/qs]

So the function of ERV's is now irrelevant?

[qs]You say: LTRs in different organisms are different.[/qs]

Nope. They are different in the same ERV in the same organism. Please read my post more carefully, as well as this paper:

"Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A). Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication."
Constructing primate phylogenies from ancient retrovirus sequences

There are two LTR's per full length ERV. They are like bookends for the viral genome. They flank both sides of the genome, and the 5' LTR serves as a strong promoter for the viral genes. When the virus inserts into the host genome the 5' and 3' LTR's are identical in sequence. The longer that an ERV stays in a genome the more differences you will find between the LTR's. Therefore, a human ERV (HERV) found in all apes will have a higher LTR divergence in the HERV than in a human ERV only found in humans and chimps (at orthologous positions). Fig 2. from the above paper shows this in spades. For example, for HERV-K(C4) the 5' LTR's group together and the 3' LTR's group together for both the orangutan and human ERV's. There is more divergence between the 5' and 3' LTR's of the human ERV than there is between the 5' LTR's between humans and orangutans. This is what we should see if evolution is true, and creationism has no way of explaining this data.

[qs]I say: They were never identical. LTRs are different based either on function and/or minor mutation. Different organisms have different physiological requirements hence LTRs are different.[/qs]

We observe that LTR's are identical when they insert into the genome. This is the observation. Are you rejecting the facts once again?

[qs]No, irrelevant. Also, nested heirarchy was already addressed.[/qs]

Nothing you have supplied explains a nested hierarchy. All you have done is point to the degree of relatedness which is nothing more than repeating the observation of a nested hierarchy. You explanation for a nested hierarchy is that species fall into a nested hierarchy. We already knew that. What I want to know is why creationism would produce a nested hierarchy, and only a nested hierarchy.
 
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Greg1234

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Sharpshooter fallacy. If we had different ERV's we would have different physiological requirements.
No, if we have different physiological reqirements we would have different ERVs.


There is nothing that requires humans as the end result, nor chimps, gorillas, bonobos, or orangutans. ERV's, if functional, produce variation, and natural selection works on that variation.

No ERVs are different because different physiological requirements means different ERVs.]

That is exactly what your functional ERV argument is leading to, that they are required for species diversification.
No, diverse physiological requirements lead to the use of different ERVs


So the function of ERV's is now irrelevant?
ERVs are established as being functional. You said some people have different elements. I said that people are different. The functions people have or lack are irrelevant to the argument where some people have different ERVs because some people are different.



Nope. They are different in the same ERV in the same organism. Please read my post more carefully, as well as this paper:


"Third, sequence divergence between the LTRs at the ends of a given provirus provides an important and unique source of phylogenetic information. The LTRs are created during reverse transcription to regenerate cis-acting elements required for integration and transcription. Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration, even if they differed in the precursor provirus (Fig. 1A). Over time, they will diverge in sequence because of substitutions, insertions, and deletions acquired during cellular DNA replication."
Constructing primate phylogenies from ancient retrovirus sequences

This was just given.
There are two LTR's per full length ERV. They are like bookends for the viral genome. They flank both sides of the genome, and the 5' LTR serves as a strong promoter for the viral genes. When the virus inserts into the host genome the 5' and 3' LTR's are identical in sequence. The longer that an ERV stays in a genome the more differences you will find between the LTR's. Therefore, a human ERV (HERV) found in all apes will have a higher LTR divergence in the HERV than in a human ERV only found in humans and chimps
This was just given.

There are two LTR's per full length ERV. They are like bookends for the viral genome. They flank both sides of the genome, and the 5' LTR serves as a strong promoter for the viral genes. When the virus inserts into the host genome the 5' and 3' LTR's are identical in sequence. The longer that an ERV stays in a genome the more differences you will find between the LTR's. Therefore, a human ERV (HERV) found in all apes will have a higher LTR divergence in the HERV than in a human ERV only found in humans and chimps (at orthologous positions). Fig 2. from the above paper shows this in spades. For example, for HERV-K(C4) the 5' LTR's group together and the 3' LTR's group together for both the orangutan and human ERV's. There is more divergence between the 5' and 3' LTR's of the human ERV than there is between the 5' LTR's between humans and orangutans. This is what we should see if evolution is true, and creationism has no way of explaining this data.
This was just given.

We observe that LTR's are identical when they insert into the genome. This is the observation. Are you rejecting the facts once again?
All LTRs are not similar. You were just arguing for your divergence via mutations among organisms. You're jumping from one thing to the other, reversing your arguments, typing superfluous speeches embedded with repetitive sequences.


Nothing you have supplied explains a nested hierarchy. All you have done is point to the degree of relatedness which is nothing more than repeating the observation of a nested hierarchy.
No, I said

1. The process has stopped which enables a hierarchy

2. I drew up my hierarchy when there were no fishes created with lungs. All fishes have gills. When fishes with lungs were created it, broke my hierarchy. Now that the creative process has generally stopped, I can look to create a hierarchy again.

3. And to add, contingency would also play a role
 
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Loudmouth

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[qs]No, if we have different physiological reqirements we would have different ERVs.[/qs]

You have already stated that ERV's have function. If they have function, as you state, then it is the ERV's that determine our physiology, not the other way around. If ERV's have function then it is ERV's that are helping to drive the appearance of differences between species, not the other way around.

To use an analogy, you are telling me that the wet spot on the ground is telling the raindrop where to fall.

ERVs are established as being functional. You said some people have different elements. I said that people are different. The functions people have or lack are irrelevant to the argument where some people have different ERVs because some people are different.

So if our physiology requires ERV's to be in a certain place why don't all humans have the same ERV's?

All LTRs are not similar.

The LTR's of a single retroviral insertion is identical at the time of insertion. That is what I am telling you, and what you continue to ignore. This is observed time and again in the lab.

[qs]You were just arguing for your divergence via mutations among organisms.[/qs]

I was just arguing for the divergence of the two LTR's of a single insertion as seen in a single organism. Here is a picture of a retroviral genome:


Notice the R's at each end? Those are the LTR's. They are identical at the time of insertion. In each generation there is a probability of a mutation occurring anywhere in that sequence, including the LTR's. This means that the R's at each end of that picture will become less and less alike over time. A recent insertion will have LTR's that are more alike than an ERV that inserted 10's of millions of years ago. The common ancestor of humans and orangutans is more distant than the common ancestor of humans and chimps. Therefore, an ERV shared by humans and orangutans should have more differences between the R's within either species compared to an ERV shared by just humans and chimps but not orangutans.

We are not comparing ERV sequences across species. We are comparing the LTR's of a single ERV in a single species. So how does creationism explain this pattern of LTR divergence?

1. The process has stopped which enables a hierarchy

No, it hasn't. Species specific mutations continue to occur, and genetic isolation continues to exist.

[qs]2. I drew up my hierarchy when there were no fishes created with lungs. All fishes have gills. When fishes with lungs were created it, broke my hierarchy. Now that the creative process has generally stopped, I can look to create a hierarchy again.[/qs]

How do fish with lungs break the nested hierarchy when evolution predicts, via the nested hierarchy, that there should have been transitional fish with a mixture of basal fish and basal tetrapod features? Do you even understand how nested hierarchies work?

[qs]3. And to add, contingency would also play a role[/qs]

Contingency of what? Humans violate the nested hierarchies with ease. For example, the Glofish is a man made species. This is a fish that carries an exact copy of a jellyfish gene, a direct violation of the nested hierarchy. If human designers can violate the nested hierarchy with ease, why couldn't God?
 
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Greg1234

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[qs]No, if we have different physiological reqirements we would have different ERVs.[/qs]

You have already stated that ERV's have function. If they have function, as you state, then it is the ERV's that determine our physiology, not the other way around. If ERV's have function then it is ERV's that are helping to drive the appearance of differences between species, not the other way around.
No, the creation of different organisms drove the elements used, not the other way around.

To use an analogy, you are telling me that the wet spot on the ground is telling the raindrop where to fall.

No, you already used the horse and cart thing. I told you that the horse and cart were in the same position. You are attempting to use the Darwinian friendly side to advance your case while ignoring the other.


So if our physiology requires ERV's to be in a certain place why don't all humans have the same ERV's?
The same reason all humans don't have the same genetic information. Notice you isolated physiological requirements from physiology to advance your case.


The LTR's of a single retroviral insertion is identical at the time of insertion. That is what I am telling you, and what you continue to ignore. This is observed time and again in the lab.

No, I listed the function of LTRs as promoters. Different functional requirements in different organisms means that there will be different LTRs. You then claimed that LTRs act as promoters in viruses which some have argued "do not eat or drink, have no metabolism with which to change anything or generate energy, no secretions, no defecation, no activities, no nerves, sensors or (electrical) nerve energy, no reproductive faculties nor, in fact, any qualities of life whatsoever." "That, as genomes, so-called viruses are merely the genetic patterns for entitative organisms with all the qualities of life as in bacteria, mitochondria, (organelles) fungi and human cells!" "Statements that so-called viruses, without any life qualities, or any ability to move or maneuver, attack cells, seize positions, inject themselves into a cell, command a cell, infect a cell, program a cell, wreak tremendous damage or in any manner perform any act or in any way cause any result are inherently absurd. The living organism always acts and causes results favorable to itself. Only pure chemical unions from chemicals (poisons) pose a serious threat. Dead materials are always acted upon! Only the living organism does the acting. The very statement that "viruses" attack when they do not have any faculties for movement, propulsion, assault or offensive action, and have no energy or capability for any activity at all and have no have no equipment for damaging anything at all, is sheer fiction."

The promotional role was most likely established by mapping viral sequences with active promoters then saying that they act as promoters in what would be, dead organic matter. In fact, as one writes "As may be expected because of the integrated phase of their life cycle, retroviruses have somewhat typical eucaryotic promoters."


You then presented reverse transcription ("Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration,") As wikipedia writes "The LTRs are partially transcribed into an RNA intermediate, followed by reverse transcription into complementary DNA (cDNA) and ultimately dsDNA (double-stranded DNA) with full LTRs. The LTRs then mediate integration of the retroviral DNA via an LTR specific integrase into another region of the host chromosome.

Retroviruses such as Human Immunodeficiency Virus (HIV) use this basic mechanism." There was actually an interesting discussion about that.

CJ: Tell me about the reverse transcriptase observations. Why don't they prove the presence of a retrovirus?

EPE: Reverse transcriptase was discovered in retroviruses, but observation of it doesn't mean you've got a retrovirus, much less one particular retrovirus, because reverse transcriptase is not the only enzyme that can reverse transcribe, and reverse transcriptase is not unique to retroviruses.

The existence of RT is proven indirectly. By putting some RNA into a culture and seeing if DNA bearing the corresponding sequence appears.​

CJ: You mean the presence of RT is implied by the ability of the culture to do this particular trick?​

EPE: Yes. It's measured by demonstrating the process of reverse transcription. Like many enzyme tests, the test for reverse transcriptase measures what the enzyme does, not the actual enzyme itself. So in the case of RT it measures the production of DNA copied from a synthetic piece of RNA introduced into the cultures. The problem is that RT is not the only thing capable of doing this trick, as you call it. Normal cellular enzymes can also do this trick. In fact, they do it very well with the same synthetic RNA that all HIV researchers introduce into their cultures to copy into DNA in order to claim that their cultures contain HIV RT, and thus HIV [24].

What's more, when you read the AIDS literature, it becomes apparent that some authors who claim to have isolated HIV have done no more than detect reverse transcription.​

CJ: So the evidence using RT does not look good?

EPE: The problem with RT is the same problem with all the evidence. It's just like the particles Gallo photographed. They might be the particles of a retrovirus. The reverse transcription might be caused by the RT of a retrovirus. But "might" is not scientific proof. You don't construct scientific theories from what "might" be going on.

CJ: How can you dismiss particles? They're very convincing. How can you escape the fact that no matter how widely Gallo and everybody else deviated from the traditional method of isolating a retrovirus, there are particles in these cultures, and a lot of very important people regard them as particles of a retrovirus.

EPE: Particles have to be viewed with a considerable amount of perspective. Retroviral-like particles are practically ubiquitous. In the 1970s such particles were frequently observed in human leukemia tissues, in cultures of embryonic tissues, and in the majority of animal and human placentas. This is of significance given that the H9 cell line is made up of leukemic cells and also because Montagnier obtained his EMs of "HIV" from cultures done with umbilical cord blood lymphocytes.

As already noted, some of these objects that look just like retroviruses are not viruses of any sort. Or they may be endogenous retroviruses. Only isolation can sort all this out.


We are not comparing ERV sequences across species. We are comparing the LTR's of a single ERV in a single species. So how does creationism explain this pattern of LTR divergence?

This was already given. LTRs are functional also. In the case of LTRs across species,

1. You are presupposing that the all the LTR elements are confined to a specific ERV suite. To put it analogically, You have a monitor, processor, keyboard and mouse in one suite. LTRs are the mouse. The keyboard, processor and monitor make up the rest of the ERV. You think that the mouse is determined by the type of keyboard, monitor and processor you have. I'm saying that the mouse is determined based on functional roles (with some chinks and scratches), independent of the keyboard etc. A particular keyboard doesn't mean that you will have a particular mouse. Some can have a standard keyboard and a laser mouse.

2. You spot an ERV suite with an infrared mouse, an infrared keyboard, 17 inch monitors, Core two duo processor. You say that this is one suite. Where ever we find an infrared keyboard, 17 inch monitors, and a core two duo processor, we should find an infrared mouse.

3. I say: The type of mouse is determined based on functional requirements (laden with a few scratches and chinks). It is not dependent on the type of keyboard, monitor etc you have.




No, it hasn't. Species specific mutations continue to occur, and genetic isolation continues to exist.
And? You are the one who thinks that this process can create a man from microbe. What's gong on here is adaptation. There is a difference among the creation of a car, the breaking down of a car, and lights on'off in a car.

How do fish with lungs break the nested hierarchy when evolution predicts, via the nested hierarchy, that there should have been transitional fish with a mixture of basal fish and basal tetrapod features? Do you even understand how nested hierarchies work?

That's completely irrelevant. Here you are just picking features. Seeing that birds are tetrapods, and Darwinian evolution depicts that fish gave rise to tetrapods, this means fishes should have feathers right? Of course, if they did, this would break the hierarchy as you have a fish with tetrapod features. But fish with tetrapod features doesn't break the hierarchy in the case of fishes with lungs because according to Darwinism, tetrapods came from fishes.



Contingency of what? Humans violate the nested hierarchies with ease. For example, the Glofish is a man made species. This is a fish that carries an exact copy of a jellyfish gene, a direct violation of the nested hierarchy. If human designers can violate the nested hierarchy with ease, why couldn't God?
This was just given. The nested hierarchy was broken multiple times.
 
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Loudmouth

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No, the creation of different organisms drove the elements used, not the other way around.

So you are saying that God inserted ERV's into the genomes and that they are not from viral infections? IOW, you are claiming that God plants fingerprints at crime scenes?

No, you already used the horse and cart thing. I told you that the horse and cart were in the same position.

Then I guess you don't understand the use of analogies. You are admitting that you are getting things out of order.

You are attempting to use the Darwinian friendly side to advance your case while ignoring the other.

The "other" is equivalent to God planting fingerprints at a crime scene. Sorry for not being convinced.

Notice you isolated physiological requirements from physiology to advance your case.

How are they different?

No, I listed the function of LTRs as promoters.

This is the exact function they have in retroviruses.

Different functional requirements in different organisms means that there will be different LTRs.

Evidence please. Please show that LTR's have to be there.

You then claimed that LTRs act as promoters in viruses . . .

And they do.

"The integrated provirus has two LTRs, and the 5' LTR normally acts as an RNA pol II promoter. The transcript begins, by definition, at the beginning of R, is capped, and proceeds through U5 and the rest of the provirus, usually terminating by the addition of a poly A tract just after the R sequence in the 3' LTR."
The LTR Retroviral Promoter

Can you please start dealing with the facts?

The living organism always acts and causes results favorable to itself.

No, it doesn't. Children are born with detrimental mutations. Retroviruses can insert into regions where there are no genes which means that they have no activity as promoters for human genes. ERV's can have both detrimental and neutral effects.

The promotional role was most likely established by mapping viral sequences with active promoters then saying that they act as promoters in what would be, dead organic matter.

The role of LTR's was established by observing real retroviruses in action. Again, these are the facts. Please deal with them.

You then presented reverse transcription ("Because of the mechanism of reverse transcription, the two LTRs must be identical at the time of integration,") As wikipedia writes "The LTRs are partially transcribed into an RNA intermediate, followed by reverse transcription into complementary DNA (cDNA) and ultimately dsDNA (double-stranded DNA) with full LTRs. The LTRs then mediate integration of the retroviral DNA via an LTR specific integrase into another region of the host chromosome.

And when the retrovirus inserts into the genome it does so randomly with respect to locus. It is not guided by the "physiological requirements" of the organism.

EPE: Reverse transcriptase was discovered in retroviruses, but observation of it doesn't mean you've got a retrovirus, much less one particular retrovirus, because reverse transcriptase is not the only enzyme that can reverse transcribe, and reverse transcriptase is not unique to retroviruses.
For full length ERV's, the whole viral genome is there including reverse trascriptase, gag, env, pro, and flanking LTR's. In fact, if you align HERV-K sequences and produce a virus with the consensus sequence you get a FUNCTIONAL RETROVIRUS.

"Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny."
Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements

It quacks like a retrovirus, it walks like a retrovirus, it swims like a retrovirus . . . What more evidence do you need that ERV's are the result of retroviral insertion?​

1. You are presupposing that the all the LTR elements are confined to a specific ERV suite. To put it analogically, You have a monitor, processor, keyboard and mouse in one suite. LTRs are the mouse. The keyboard, processor and monitor make up the rest of the ERV. You think that the mouse is determined by the type of keyboard, monitor and processor you have. I'm saying that the mouse is determined based on functional roles (with some chinks and scratches), independent of the keyboard etc. A particular keyboard doesn't mean that you will have a particular mouse. Some can have a standard keyboard and a laser mouse.

That is not what I am saying at all. I am saying that the divergence of the two LTR's in a single ERV is due to the amount of time in the lineage. You have brought nothing forward to refute this.

And? You are the one who thinks that this process can create a man from microbe.

Please address my response. Divergence continues today. It will continue to occur as long as species reproduce and do not pass genes between species.

What's gong on here is adaptation.

Natural selection of ERV's occurs after they are inserted. Since ERV's insert randomly, different species will have different ERV's to select from. This is what drives divergence.

That's completely irrelevant. Here you are just picking features. Seeing that birds are tetrapods, and Darwinian evolution depicts that fish gave rise to tetrapods, this means fishes should have feathers right?

Again, do you know how nested hierarchies work? It appears not. Feathers are a derived trait that evolved in the dinosaur lineage after basal tetrapods diversified. No one in their right mind would pose such a question if they understood biology. All you are doing is airing your ignorance of biology. Please, learn cladistics and how it applies to our discussion. Otherwise, you will keep making a fool of yourself like you did in the quote above.

What would break the nested hierarchy is an organism with derived bird and mammalian features. A bat with feathers or a bird with three middle ear bones would make nice examples. So what was stopping God from creating species like a flying animal with feathers and teats, or a flying animal with feathers and three middle ear bones? Care to explain?

The nested hierarchy was broken multiple times.

You obviously don't understand how a nested hierarchy would be broken.
 
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Astridhere

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And physiological requirements dictate which ERV elements are needed to perform the task. The cart and the horse are at the same position.

No I'm not. You are.


This was geared toward the random integration argument.




Irrelevant.




I'll simplify it this time. Maybe you can get it. \

You say: LTRs in different organisms are different. But they were all identical upon insertion within some common ancestor. When the common ancestor mutated, thats how the differences arose.

I say: They were never identical. LTRs are different based either on function and/or minor mutation. Different organisms have different physiological requirements hence LTRs are different.

You say: Humans and other humans and humans and chimps share a higher degree of LTR similarity between them because divergence between humans is low.

I say: Humans share a high degree of LTR similarity because they have a high degree of functional similarities.

You say: There is more divergence in the LTR's of human ERV's that are shared by all apes

I say: LTRs which are shared by all apes cover a more physiologically diverse ground and hence would be less similar to each other.



No, irrelevant. Also, nested heirarchy was already addressed.


No it wasn't.


This was just given.

Thanks heaps for the responses to my questions. This post particularly is fantastic for me with no science background. My degree is in the social sciences, not quite the same thing.

I just want to say that I believe you have made your point time and again. This is all theoretical and you have proposed a creationist paradigm that is just as robust as any evolutionary one.

Human ERV-K had a similar demographic signature to that of the rhesus monkey, both differing greatly from that of the chimpanzee. The evolutionary explanation is 'purging'. Your explanation would be simply that rhesus monkey and humans share this similarity likely due to similar function, not ancestry with the added convolution of necessary purging to make the data fit the evolutionry paradigm.

Well done Greg1234! Yours is the more parsinomous explanation.

DNA Chunks, Chimps And Humans: Marks Of Differences Between Human And Chimp Genomes

ScienceDaily (Nov. 6, 2008)

"It is evident that there has been striking turnover in gene content between humans and chimpanzees, and some of these changes may have resulted from exceptional selection pressures," explains Dr George Perry from Arizona State University and Brigham and Women's Hospital, another leading author of the study. "For example, a surprisingly high number of genes involved in the inflammatory response - APOL1, APOL4, CARD18, IL1F7, IL1F8 - are completely deleted from chimp genome. In humans, APOL1 is involved in resistance to the parasite that causes sleeping sickness, while IL1F7 and CARD18 play a role in regulating inflammation: therefore, there must be different regulations of these processes in chimpanzees.

CNVs in humans and chimpanzees often occur in equivalent genomic locations: most lie in regions of the genomes, called segmental duplications, that are particularly 'fragile'. However, one in four of the 355 CNDs that the team found do not overlap with CNVs within either species - suggesting that they are variants that are 'fixed' in each species and might mark significant differences between human and chimpanzee genomes."


This information correlates with your theory and assertions. However this is about what is not shared. This research demonstrates that mankind has its own system of inflamation regulation that must be different to chimps. 'Evolutionary selection' is the evolutionary explanation. However, a non ancestral connection is once again the more parsinomous explanation.

Thanks again for your responses. They have clarified your argument, which appears to be quite valid.
 
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Loudmouth

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This is all theoretical and you have proposed a creationist paradigm that is just as robust as any evolutionary one.

Then perhaps you can help me with this. How does the creationist paradigm explain the nested hierarchy produced by overall ERV divergence, LTR divergence, and the pattern of orthology. These are the 3 phylogenetic signals that MG spoke of in the OP. I have yet to see any creationist explain how their paradigm produces this pattern.

Human ERV-K had a similar demographic signature to that of the rhesus monkey, both differing greatly from that of the chimpanzee. The evolutionary explanation is 'purging'. Your explanation would be simply that rhesus monkey and humans share this similarity likely due to similar function, not ancestry with the added convolution of necessary purging to make the data fit the evolutionry paradigm.

Using the creationist paradigm, can you predict how many of those ERV-K insertions are found at the same position in the human and rhesus monkey genomes?

DNA Chunks, Chimps And Humans: Marks Of Differences Between Human And Chimp Genomes

ScienceDaily (Nov. 6, 2008)

"It is evident that there has been striking turnover in gene content between humans and chimpanzees, and some of these changes may have resulted from exceptional selection pressures,"

This directly refutes Greg's position and supports mine. I have been saying from the start that ERV's insert first, and then they are put through natural selection. Greg disagrees with me, and the author you are quoting. You also missed this quote:

"CNDs are likely to include genes that have influenced evolution of each species since humans and chimpanzees diverged some six million years ago."

DNA Chunks, Chimps And Humans: Marks Of Differences Between Human And Chimp Genomes

Oops, not so friendly for Greg, is it. This is exactly what I have been saying all along, and what Greg has disagreed with. Thank you for finding a paper that finally settles it.
 
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Astridhere

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Every time? I would like to see any references you have which demonstrate that random mutations are detrimental each and every time.

BTW thanks for your responses also. I understand this is all theoretical. The point for me being that evolutionists strongly purport that their assertions are the only ones that carry any validity. I see that Steve1234, although offering another theory to explain the data, has demonstrated that creationists explanations are there and have as strong a theoretical base as evolutionary ones.

Even I know in Drosophila 70% of the mutations were detrimental. What were the 30% that were not? If these simply relate to microevolutionary adaptations, that no one disagrees with, such as immunity, size, colour etc it demonstrates that there are limits to adapatation.

Just because a fruitfly can grow legs off its head and die, does not mean a cold blooded lizard can become a warm blooded bird or that ERV's can change functions during evolution. ERVs are not intelligent. They are dead elements as Greg1234 pointed out.

One oft-cited "beneficial" mutation is bacterial antibiotic resistance. Yet antibiotic resistance does not introduce new information into the genome (see right). This is [FONT=Arial,Arial][FONT=Arial,Arial]microevolution [/FONT][/FONT]because it involves only minor change "within a species" and does not add information. Antibiotic resistance is not [FONT=Arial,Arial][FONT=Arial,Arial]macroevolution [/FONT][/FONT]and does not explain how new biological structures arise; it never results in one bacterial species becoming another. Interestingly, antibiotic resistant bacteria face a net "fitness cost" and are weakened by the very mutation that made them drug-resistant.
(IDEA - Mutations in a Nutshell)

So Greg1234 appears to make a valid statement that appears to only be challenged by evolutionary assumptions rather than factual data.
 
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Loudmouth

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The point for me being that evolutionists strongly purport that their assertions are the only ones that carry any validity.

In this thread, it is certainly true. Greg has even gone to the point of sayign that ERV's were not created by retroviruses. To use my analogy, he is arguing that God puts the defendant's fingerprints at crime scenes. Sorry, but that is not a valid argument. ERV's are the fingerprints of retroviral insertion.

On top of that, the pattern of similarities and differences seen in ERV's is the exact pattern that the theory of evolution predicts that we should see. Greg has never even tried to prove this wrong. Instead, he has made vague allusions to "physiological requirements" that do not explain the nested hierarchy. IOW, the creationist explanation does not explain the facts. It is the facts that are important here, and Greg is ignoring the facts.

I see that Steve1234, although offering another theory to explain the data, has demonstrated that creationists explanations are there and have as strong a theoretical base as evolutionary ones.

The creationist explanations have not addressed the facts, therefore they have a very weak theoretical base. The fact is that there are 3 levels of ERV sequence data that fall into a nested hierarchy, the very pattern that evolution predicts should be there. Creationists have yet to demonstrate why we see this pattern, and no other pattern. Greg even goes as far as arguing that it doesn't exist. Ignoring the facts is the antithesis of a solid theory.

Even I know in Drosophila 70% of the mutations were detrimental.

Reference?

You were born with 100 to 200 mutations. How many of those do you think are detrimental?


Just because a fruitfly can grow legs off its head and die, does not mean a cold blooded lizard can become a warm blooded bird or that ERV's can change functions during evolution. ERVs are not intelligent. They are dead elements as Greg1234 pointed out.

So you are saying that the differences between humans and chimps is NOT due to a difference in DNA, with ERV's making up some of those differences? You disagree with the very paper that you referenced?

One oft-cited "beneficial" mutation is bacterial antibiotic resistance. Yet antibiotic resistance does not introduce new information into the genome (see right). This is [FONT=Arial,Arial][FONT=Arial,Arial]microevolution [/FONT][/FONT]
because it involves only minor change "within a species" and does not add information. Antibiotic resistance is not [FONT=Arial,Arial][FONT=Arial,Arial]macroevolution [/FONT][/FONT]and does not explain how new biological structures arise; it never results in one bacterial species becoming another. Interestingly, antibiotic resistant bacteria face a net "fitness cost" and are weakened by the very mutation that made them drug-resistant.
(IDEA - Mutations in a Nutshell)

So more of the creationist "no new information" and "microevolution" obsfucations. Sorry, but this is why ID and creationism is not considered science. Every mutation is new information, whether it is beneficial or not. All of evolution is microevolution.

So Greg1234 appears to make a valid statement that appears to only be challenged by evolutionary assumptions rather than factual data.

The theory of evolution makes PREDICTIONS, and the data mimics those predictions. The creationist model makes NO PREDICTIONS, and therefore can not claim that it fits the data. Nowhere has Greg explained why creationism would produce a nested hierarchy, and a nested hierarchy only. Therefore, he can not claim that the data fits his theory.
 
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Astridhere

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Then perhaps you can help me with this. How does the creationist paradigm explain the nested hierarchy produced by overall ERV divergence, LTR divergence, and the pattern of orthology. These are the 3 phylogenetic signals that MG spoke of in the OP. I have yet to see any creationist explain how their paradigm produces this pattern.

I will leave the specifics to someone with the credentials to refute. Greg1234 has. My take on it is this.

Phylogenetic Signal, Evolutionary Process, and Rate 2008

"In this study, we use individual-based numerical simulations on stochastic phylogenetic trees to clarify the relationship between phylogenetic signal, rate, and evolutionary process. Under the simplest model for quantitative trait evolution, homogeneous rate genetic drift, there is no relation between evolutionary rate and phylogenetic signal. For other circumstances, such as functional constraint, fluctuating selection, niche conservatism, and evolutionary heterogeneity, the relationship between process, rate, and phylogenetic signal is complex. For these reasons, we recommend against interpretations of evolutionary process or rate based on estimates of phylogenetic signal."



All this is based on the assumption of evolution. Indeed some organism is bound to be more similar to another, both genetically and morphologically. If chimps had not have made it then it would be something else. If all apes went extinct then it would be something else. It appears to be no more than a game researchers like to waste their time on based on an evolutionary assumption.


Using the creationist paradigm, can you predict how many of those ERV-K insertions are found at the same position in the human and rhesus monkey genomes?

There is not need to predict anything I do not think. Certainly many evo predictions have failed and that apparently does not invalidate TOE. The question is how many times did the creator recycle a great idea?

This directly refutes Greg's position and supports mine. I have been saying from the start that ERV's insert first, and then they are put through natural selection. Greg disagrees with me, and the author you are quoting. You also missed this quote:
This is theoretical and contains maybes, and says nothing to support your position at all. It says nothing as to HOW ERVs got there. Rather it says only half occur in the same region...which is a long shot from most. According to Greg, I think, this this simply reflects we may share some functional similarity as a human can with a rhesus monkey and not a chimp. It all aligns nicely with creation.

If the same ERV in the same region performs a different fuction, all the more would it refute common descent. ERVs have no intelligence and do not know to change function without it being a part of the creative directive to do so.
"CNDs are likely to include genes that have influenced evolution of each species since humans and chimpanzees diverged some six million years ago."

DNA Chunks, Chimps And Humans: Marks Of Differences Between Human And Chimp Genomes

Oops, not so friendly for Greg, is it. This is exactly what I have been saying all along, and what Greg has disagreed with. Thank you for finding a paper that finally settles it.

I disagree. The problem for you is that anything provides support for TOE, no matter of the fact that the new data challenges former expectations. It does not matter what you find in connection to ERV's, there will always be some convoluted explanation as this, like the rest, is unfalsifiable. When you thought ERV's were functionless that 'proved' common descent. Now you are finding ERVs have function and this still proves common descent, does it?. Even the social sciences can do better than this.


"It is evident that there has been striking turnover in gene content between humans and chimpanzees, and some of these changes may have resulted from exceptional selection pressures,"


MAY, LIKELY and PERHAPS are not facts.

"One of the genes affected by CNVs is CCL3L1, for which lower copy numbers in humans have been associated with increased susceptibility to HIV infection. Remarkably, the study of 60 human and chimpanzee genomes found no evidence for fixed CNDs between human and chimp and no within-chimp CNV. Rather, they found that a nearby gene called TBC1D3 was reduced in number in chimpanzee compared to human: typically, there were eight copies in human, but apparently only one in all chimpanzees".

So this smacks of ancestry to you. For me mankind has been given a moral standard and the creation of mankind with an ability to be infected by a sexually transmitted disease, that apes are immune to, is a reflection of the recompense God has written into our genetic code to provide consequences in this life for immoral behaviour. This is a result of creation, not evolution.

Let's not forget that a creationists prediction is there is no junk DNA, ervs included. Junk DNA was always held as evidence against creation. The data continues to suppport the creationist assertion without the need for knee jerk continual changes to it. If the validation of theory is meant to be demonstrated by more data, then the creationists hold the prize on this one!

Greg1234 has provided an excellent refute to ERV's being irrefuteable evidence for common descent and demonstrated as sound a theoretical base as any evo one.
 
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Astridhere

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In this thread, it is certainly true. Greg has even gone to the point of sayign that ERV's were not created by retroviruses. To use my analogy, he is arguing that God puts the defendant's fingerprints at crime scenes. Sorry, but that is not a valid argument. ERV's are the fingerprints of retroviral insertion.

On top of that, the pattern of similarities and differences seen in ERV's is the exact pattern that the theory of evolution predicts that we should see. Greg has never even tried to prove this wrong. Instead, he has made vague allusions to "physiological requirements" that do not explain the nested hierarchy. IOW, the creationist explanation does not explain the facts. It is the facts that are important here, and Greg is ignoring the facts.



The creationist explanations have not addressed the facts, therefore they have a very weak theoretical base. The fact is that there are 3 levels of ERV sequence data that fall into a nested hierarchy, the very pattern that evolution predicts should be there. Creationists have yet to demonstrate why we see this pattern, and no other pattern. Greg even goes as far as arguing that it doesn't exist. Ignoring the facts is the antithesis of a solid theory.



Reference?

You were born with 100 to 200 mutations. How many of those do you think are detrimental?

I am still human like my mum!



So you are saying that the differences between humans and chimps is NOT due to a difference in DNA, with ERV's making up some of those differences? You disagree with the very paper that you referenced?
Misrepresenting what I say will get you nowhere


So more of the creationist "no new information" and "microevolution" obsfucations. Sorry, but this is why ID and creationism is not considered science. Every mutation is new information, whether it is beneficial or not. All of evolution is microevolution.



The theory of evolution makes PREDICTIONS, and the data mimics those predictions. The creationist model makes NO PREDICTIONS, and therefore can not claim that it fits the data. Nowhere has Greg explained why creationism would produce a nested hierarchy, and a nested hierarchy only. Therefore, he can not claim that the data fits his theory.



A weak theoretical base is demonstrated by ever changing theories. I am afraid your evo theories are the prize winners here. Common descent is built on a foundation of straw and therefore topples at the slightest breeze. eg ERV functionality.

Your nested heirarchies have been addressed. Just because you do not like the explanation does not mean it has not been satisfactorily addressed.

Life today can be categorised. When you are trying to show common descent from fossils millions of years old we are on a new level that evokes assumptions. What nested heirarchy does Ardi, have with mankind now that he has been railroaded into an ape ancestor and not a human one. What about Lucy with gorilla features and Turkana Boy with his small neural canal? Are these in nested heirarchies?

If you want to believe in common descent, based on all this, eg. that a hippo is closer to a whale than a pig is, that Indohyus is closer to a whale than Indohyus is to a mouse deer alive today; that abulocetus natans is closer to a whale than a crocodile, that is just dandy. However it is all speculation and I think based on very erraneous assumptions.

Even as a layperson in science I can see that these nested heirarchies of yours mean nothing and are based on assumptions, misrepresentation, acceptence of theories that constantly change, population size and bottlenecks and complicated algorithms, and really says nothing at all about sharing a common ancestor with chimps or bacteria.
 
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Loudmouth

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I will leave the specifics to someone with the credentials to refute. Greg1234 has.


Where did he refute it?

[qs]
Phylogenetic Signal, Evolutionary Process, and Rate 2008 . . .[/quote]

From that very same paper:

"If one’s goal is to assess the evolutionary process underlying the distribution of character states among species, a better approach might be to consider fitting alternative models for the evolutionary process to the data and tree. . .Such models include punctuational divergence (Oakley et al. 2005; Lee et al., 2006), accelerating and decelerating evolutionary rate (Blomberg et al., 2003), and explicitly adaptive models for niche occupancy and evolution (Butler and King, 2004)."

What they are talking about is different modes of evolution and how they impact the phylogenetic signal.

There is not need to predict anything I do not think.


Then you don't even have a theory. Theories make predictions. You are saying that there is a creationist theory that explains orthologous and non-orthologous ERV's, and yet when asked to address the evidence you refuse to say what the theory predicts as to the very thing it is supposed to explain. Do you see a problem here?

Certainly many evo predictions have failed and that apparently does not invalidate TOE. The question is how many times did the creator recycle a great idea?


How many times would the Creator need to recycle an idea, and why would they necessarily fall into a nested hierarchy? How many times have I asked this now?

This is theoretical and contains maybes, and says nothing to support your position at all. It says nothing as to HOW ERVs got there.


Have you been reading this thread? We have already shown how ERV's get into genomes. They get there through retroviral insertion.

According to Greg, I think, this this simply reflects we may share some functional similarity as a human can with a rhesus monkey and not a chimp.


Are these ERV's found at orthologous positions? Are you even considering the pattern of orthology, LTR divergence, or overall sequence divergence? If not, then you are not even dealing with our argument, much less refuting it.

It all aligns nicely with creation.

Why does a nested hierarchy align nicely with creation? You still haven't explained this?

If the same ERV in the same region performs a different fuction, all the more would it refute common descent.


Why? Evolution is descent with modification. So you are arguing that descent with modification actually refutes evolution? Really?

ERVs have no intelligence and do not know to change function without it being a part of the creative directive to do so.


You are aware that mutations change function, right?

The problem for you is that anything provides support for TOE, no matter of the fact that the new data challenges former expectations.

You should really reread my previous posts. I list several potential pieces of evidence that would NOT support the TOE. Birds with teats and bats with feathers are two perfect examples. We can also add potential ERV evidence. If ERV's did not fall into a nested hierarchy then it would NOT support the TOE. That's the whole point. The TOE predicts a specific pattern, and that pattern was observed. Is it my fault that the TOE keeps passing these tests? Is it my fault that creationism is incapable of making these types of predictions?

It does not matter what you find in connection to ERV's, there will always be some convoluted explanation as this, like the rest, is unfalsifiable.

And the ultimate creationist excuse has been unfurled. Sorry, but the evidence is what it is. That is the evidence we are dealing with. It matches the predictions made by the theory of evolution. You don't get to invent imaginary falsifying evidence in order to ignore the real evidence. Surely you know this?

When you thought ERV's were functionless that 'proved' common descent.

Whether or not ERV's have function HAS NOTHING TO DO WITH MY ARGUMENT. If you actually understood my argument you would know this. Even if every ERV has function the argument is unchanged. It is still valid. The argument has to do with the phylogenetic signal in the ERV's, not their function. Even if every ERV had function THEY WOULD STILL FORM THE SAME NESTED HIERARCHY, THE SAME NESTED HIERARCHY THAT CREATIONISM CAN NOT EXPLAIN.

Tell you what. Why don't you tell us what pattern of orthology, LTR divergence, and overall ERV sequence divergence we should see if evolution is true. Since you don't think this evidence points to evolution, why don't you tell us what real evidence would look like. Can you do it?

Let's not forget that a creationists prediction is there is no junk DNA, ervs included.

Then creationism has already lost. There is tons of confirmed junk DNA. Scientists even removed millions of base pairs of junk DNA from mice, and they were unaffected. Pseudogenes such as the human GULO pseudogene are definitely junk.

Junk DNA was always held as evidence against creation.

Why shouldn't it, given your claim that creationism predicts that there should be no junk DNA. Are you saying that we are not allowed to test creationism?

Greg1234 has provided an excellent refute to ERV's being irrefuteable evidence for common descent and demonstrated as sound a theoretical base as any evo one.

You can't claim this until you show how creationism can predict a nested hierarchy. You haven't yet, so your assertions are without evidence.
 
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Nostromo

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Your nested heirarchies have been addressed. Just because you do not like the explanation does not mean it has not been satisfactorily addressed.
Yeah, you and the other guy who knows nothing about the subject just blew 150 years of evidence out of the water in a dozen posts on an Internet forum. I'll let you know when the Australian Academy of Science have set a date for the award ceremony.
 
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