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The Great Syncytin Challenge To Intelligent Design


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#41 Salsa

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Posted 20 September 2013 - 12:20 AM

Some retroviruses perform functions within the body, but where they do, it is only part of the ERV that does anything. Other ERVs do nothing, and yet others are implicated in late-onset diseases such as cancers. A 'designer' hypothesis that 'explains' positive function and no function and detrimental function points to a very strange designer.

 

Barry, there is a huge flaw in that kind of reasoning. When you go to a junkyard you might find cars that are functional, do not function, and that if driven would prove to be "detrimental". Does that reflect on the characteristics of the designer? 



#42 Barry Desborough

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Posted 20 September 2013 - 12:40 AM

Barry, there is a huge flaw in that kind of reasoning. When you go to a junkyard you might find cars that are functional, do not function, and that if driven would prove to be "detrimental". Does that reflect on the characteristics of the designer? 

The junkyard is a junkyard of retroviral genes, the original function of which was to replicate viruses.



#43 FaithfulCenturion

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Posted 20 September 2013 - 12:42 AM

In case anyone was wondering, ol' Barry here has been smacked down numerous times on the other forum he linked to. (I did a quick perusal of his posting history there) What's that saying about doing the same thing over and over while expecting a different result? ;)

#44 Barry Desborough

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Posted 20 September 2013 - 01:59 AM

In case anyone was wondering, ol' Barry here has been smacked down numerous times on the other forum he linked to. (I did a quick perusal of his posting history there) What's that saying about doing the same thing over and over while expecting a different result? wink.png

I'd love to hear what you consider to be a "smackdown"! :D



#45 Barry Desborough

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Posted 20 September 2013 - 02:04 AM

For some reason I cannot break the quote up with spaces so will revert to my old style with numbers.

 

 

1. Claiming its concluded doesn't stop it being assumed. Unless you can experimentally demonstrate in real time what you claim then it is an assumption, plain and simple.

 

2. Virtually identical... Meaning there are differences? Hmmm.

I do wonder that if this is the case wouldn't such be evidence against mutation changes in the genome. The current method of DNA analysis includes adding insertions into the DNA being assessed due to the assumption that millions of years of mutations have occured and thus the DNA would be different. If this is the case then shouldn't the ERVs also be different also?

So on one hand evolutionists claim differences are caused by mutation and thus evidence of evolution, yet in this case evolutionists claim they are similar and therefore are evidence of evolution.

 

Additionally I wonder how can one determine what is an ERV in our DNA or not?



3. And how was this "majority vote" conducted, I hope you excuse me since too many times I have seen evolutionist scientists take "liberties" in their studies in order to attempt to prove their evolutionist dogma, (see piltdown man, nebraska man, java man, Lucy, Haekle, etc).

 

4. Which doesn't explain the chicken and the egg conundrum I mentioned twice before.

 

5. This is merely your opinion and is not a point for anything.

 

6. And? That doesn't support evolutionary origins only that viruses can become endogenous which is what you claimed before

 

So what DNA sequences have been looked at and which ERVs are similar with which other ones?

I prefer numbers. Several points here. Will get back to you as soon as I can.



#46 Adam Nagy

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Posted 20 September 2013 - 02:55 AM

Barry, why not answer my question? You want to convince us how it must be impossible for chimps and humans to have the same segment of virally effected code (assuming we 'know' this is the reason for its current state) without common ancestry, right?

If this is meant to be the death knell for creationist arguments that chimps and humans are different kinds, then if these 'low chances' are meant to be so important then what does that say about the chances of abiogenesis, convergent evolution, etc...?

If you'd like I'll start a new thread but I don't think this is unrelated to the topic since you appear to be convinced that there is no chance that two organisms could develop assumed flaws in their genes in the same spot for the same reason without common ancestry.

#47 Calypsis4

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Posted 20 September 2013 - 05:26 AM

As much as I agree with you Calypsis I think we should stick to the original topic for this thread. It does no good to anyone by chasing rabbit-holes since Barry may possibly feel cheated since he came here wanting an answer to his specific question.

Gotcha. I guess my mind is stuck in 'first things first'. If one can't get to first base he'll never make it to home plate.

But, do you think he will accept any answer you give him on the matter?

#48 Barry Desborough

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Posted 20 September 2013 - 06:35 AM

For some reason I cannot break the quote up with spaces so will revert to my old style with numbers.

 

 

1. Claiming its concluded doesn't stop it being assumed. Unless you can experimentally demonstrate in real time what you claim then it is an assumption, plain and simple.

 

2. Virtually identical... Meaning there are differences? Hmmm.

I do wonder that if this is the case wouldn't such be evidence against mutation changes in the genome. The current method of DNA analysis includes adding insertions into the DNA being assessed due to the assumption that millions of years of mutations have occured and thus the DNA would be different. If this is the case then shouldn't the ERVs also be different also?

So on one hand evolutionists claim differences are caused by mutation and thus evidence of evolution, yet in this case evolutionists claim they are similar and therefore are evidence of evolution.

 

Additionally I wonder how can one determine what is an ERV in our DNA or not?



3. And how was this "majority vote" conducted, I hope you excuse me since too many times I have seen evolutionist scientists take "liberties" in their studies in order to attempt to prove their evolutionist dogma, (see piltdown man, nebraska man, java man, Lucy, Haekle, etc).

 

4. Which doesn't explain the chicken and the egg conundrum I mentioned twice before.

 

5. This is merely your opinion and is not a point for anything.

 

6. And? That doesn't support evolutionary origins only that viruses can become endogenous which is what you claimed before

 

So what DNA sequences have been looked at and which ERVs are similar with which other ones?

I prefer numbers too.

 

1. Claiming something is being assumed does not mean that it is. We can experimentally demonstrate what we know about retroviruses and ERVs.

 

2. As I said before, you would not want a fully functional provirus embedded in every cell of your body. Reverse transcription is a very error-prone process, and often fails to produce a functional provirus. See the reference to the phoenix virus for the types of errors encountered in ERVs. It's the usual stuff. Substitutions, insertions and deletions.

 

Mutation rates to nuclear DNA are a different topic. I'm happy to discuss the issue. Maybe in another thread.

 

We can determine what is an ERV by the signs I described earlier. Repetition of a short stretch of native DNA either side of the integration site, long term repeats at each end, signature retroviral genes such as reverse transcriptase and integrase, which are only of  any use to a retrovirus. It doesn't take much reverse transcription error and subsequent mutation to render this DNA ineffective, but It is still easily recognizable. In fact, the 200,000 figure is probably an underestimate. Some older ERVs could well be mutated to the point where it is difficult to be sure they are of retroviral origin. The 200,000 we can be pretty sure of. A handful would be a clincher for common descent, if they were found in corresponding locations in two different species, but we are getting ahead of ourselves. At this point, I am merely explaining why ERVs are concluded to have been of retroviral origin.

 

3. The majority vote in the Phoenix virus experiment is described in the paper, Identification of an infectious progenitor for the multiple-copy HERV-K human endogenous retroelements  I explain the process by analogy here, The Phoenix Virus.

 

4. A marsupial that provides a bit more nurturing in the womb will produce fitter offspring, and their progeny, in turn, if they develop an even more advantageous pre-birth environment, will also meet with more reproductive success. It's not an either/or thing. A fully developed placental system "poofing" into existence would falsify evolution. It is not how evolution occurs. 

 

5. It doesn't matter what phenomena we find. We can always claim that an omni-everything designer did it, for reasons we do not have to explain. But that cannot explain why anything is one way and not another, so it has no explanatory power. It cannot explain, for example, why a syncytin-bearing ERV includes reverse transcriptase and integrase. This is the question raised in the OP, and nobody so far has offered at even a suggestion for an explanation. Endogenization does just that. It fits all the observed data and makes complete sense.

 

6. I'm glad you agree that retroviruses can become endogenized. That is one of the contributory items in the case for common descent, a case which I have not made yet. I am not assuming evolution here. 

 

Go and look at the original Phoenix virus paper for examples of several similar ERV sequences. If you want to see more, there is a whole zoo of them. Just get googling.



#49 Barry Desborough

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Posted 20 September 2013 - 06:45 AM

Barry, why not answer my question? You want to convince us how it must be impossible for chimps and humans to have the same segment of virally effected code (assuming we 'know' this is the reason for its current state) without common ancestry, right?

If this is meant to be the death knell for creationist arguments that chimps and humans are different kinds, then if these 'low chances' are meant to be so important then what does that say about the chances of abiogenesis, convergent evolution, etc...?

If you'd like I'll start a new thread but I don't think this is unrelated to the topic since you appear to be convinced that there is no chance that two organisms could develop assumed flaws in their genes in the same spot for the same reason without common ancestry.

I'm not ready to explain that yet. We need to establish the background evidence first.

 

It is not possible to estimate the probability of abiogenesis. For that, we need data. It is not available. For ERVs, we can fairly easily estimate the probability  of coincidence (it is infinitesimal), but we are not ready to look at that evidence just yet. Re. convergence, I see it as supporting evidence for evolution, but that is not our topic. If the probability of coincidental integrations is infinitesimal, that is not affected by probability measures of anything else. The probability of my winning the lottery today is unaffected by the probability of being run over by a truck tomorrow.

 

We don't need a new thread. I shall be explaining the probability estimates in due course.



#50 Salsa

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Posted 20 September 2013 - 08:28 AM

The junkyard is a junkyard of retroviral genes, the original function of which was to replicate viruses.

 

No, the junkyard is a junkard. Period. How do you know what the "original function" was? Were you there?



#51 Barry Desborough

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Posted 20 September 2013 - 08:39 AM

No, the junkyard is a junkard. Period. How do you know what the "original function" was? Were you there?

Haven't you been reading my posts? ERVs exhibit a trace of insertion - a repeat of native DNA either side of it, and are additionally bracketed by retroviral long term repeats. This is what retroviral integrase does. ERVs include DNA for environment genes, integrase itself and reverse transcriptase. These are all retroviral genes, seen in action in operational retroviruses. ERVs have been resurrected as fully working retroviruses. Retroviruses are observed becoming ERVs in koalas. ERVs are the inherited remnants of retroviral integrations into ancestral germlines.



#52 Barry Desborough

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Posted 20 September 2013 - 09:19 AM

Syncytins are proteins involved in the attachment of the placenta to the uterus. They perform a very similar function to retroviral env genes that have the function of attaching a virus particle to a host cell that a retrovirus is infecting. It is not necessary, from a design PoV, to embed the DNA for these syncytins in an endogenous retrovirus (ERV), the remaining DNA of which serves no function. It is sufficient to have such proteins coded for without the ERV baggage. Indeed, in many species, this is what we see. Yet, often, syncytins are to be found in such situations. Why? The scientific explanation is that species that had received a germ-line integration of the retroviruses that gave rise to the ERV-embedded syncytins just happened to benefit from this particular gene, which was either an original mutation of the env gene involved - an error in reverse-transcription, which is known to be error-prone - or a subsequent mutation of the integrated gene.

If there is an alternative design explanation? What could it be?

OK, I think that everyone has had a good chance to come up with their ideas about why syncytins appear in ERVs. Mine follows.

 

A syncytin is a protein that allows cells to fuse together to form a syncytium, which is a fusion of single-nucleus cells to form effectively a single large cell with multiple nuclei. There is more detail at the link, which is to a Wikipedia entry.

 

Another important vertebrate syncytium is in the placenta of placental mammals. Embryo-derived cells that form the interface with the maternal blood stream fuse together to form a multi-nucleated barrier. This is probably important in order to limit the exchange of migratory cells between the developing embryo and the body of the mother, as someblood cells are specialized to be able to insert themselves between adjacent epithelial cells. The syncytial epithelium of the placenta does not provide such an access path from the maternal circulation into the embryo.

Syncytia can also form when cells are infected with certain types of viruses, notably HIV and paramyxoviruses, e.g. respiratory syncytial virus (RSV). During infection, viral fusion proteins used by the virus to enter the cell are transported to the cell surface where they can cause the host cell membraneto fuse with neighbouring cells.

HIV infects CD4+ T cells and makes the cell produce viral proteins, including fusion proteins. Then, the cell begins to display surface HIV glycoproteins, which are antigenic. Normally, a cytotoxic T cell will immediately come to "inject" lymphotoxins, such as perforin or granzyme, that will kill the infected T helper cell. However, if there are nearby T helper cells, the gp41 HIV receptors displayed on the surface of the T helper cell will bind to other similar lymphocytes.[6] This makes dozens of T helper cells fuse cell membranes into a giant, nonfunctional syncytium, which allows the HIV virion to kill many T helper cells by infecting only one.

So syncytium formation is a natural "strategy" of certain retroviruses. Fusion proteins operate on certain cell types, recognized by their surface proteins. Certain environmental triggers will time their action. It is not difficult to envisage small changes to viral regulators and fusion proteins so that it causes the formation of the syncytial epithelium at the right time of development. As I have already said, there are different syncytins in different ERVs in different positions in the genomes of different placental lineages. This sort of thing has happened many times. I shall be presenting evidence that shows that different syncytins from different ERVs have gone in and out of use in the history of these lineages. 



#53 Salsa

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Posted 20 September 2013 - 09:34 AM

Haven't you been reading my posts? ERVs exhibit a trace of insertion - a repeat of native DNA either side of it, and are additionally bracketed by retroviral long term repeats. This is what retroviral integrase does. ERVs include DNA for environment genes, integrase itself and reverse transcriptase. These are all retroviral genes, seen in action in operational retroviruses. ERVs have been resurrected as fully working retroviruses. Retroviruses are observed becoming ERVs in koalas. ERVs are the inherited remnants of retroviral integrations into ancestral germlines.

 

Sure, but since you are questioning the intention of the designer and implying that you understand the original function was then I expect you to give an account of what that function was.



#54 Barry Desborough

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Posted 20 September 2013 - 09:41 AM

Sure, but since you are questioning the intention of the designer and implying that you understand the original function was then I expect you to give an account of what that function was.

Oh, so it's one rule for you, and another for me? You don't have to explain anything, but I have to explain everything? What do you think the original function of the reverse transcriptase was? What about the integrase?

 

I have already given  you an account of what the original function was. We can see it today in active retroviruses. Invade a cell, reverse transcribe the RNA genome into DNA, insert the DNA into the cells own nuclear DNA. The cell then makes new retroviruses.

 

I'm not questioning the intention of any designer. I'm asking you what you imagine your hypothetical designer's intention was.



#55 Salsa

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Posted 20 September 2013 - 09:57 AM

Oh, so it's one rule for you, and another for me? You don't have to explain anything, but I have to explain everything? What do you think the original function of the reverse transcriptase was? What about the integrase?

 

I have already given  you an account of what the original function was. We can see it today in active retroviruses. Invade a cell, reverse transcribe the RNA genome into DNA, insert the DNA into the cells own nuclear DNA. The cell then makes new retroviruses.

 

I'm not questioning the intention of any designer. I'm asking you what you imagine your hypothetical designer's intention was.

 

Your comment that "None of this can be made any sense of by a 'designer' hypothesis" implies that you are "questioning the intention of the designer", n'est pas?

 

I don't need to supply the intention of the designer unless it can be pointed out that it actually IS the intention of the designer. 



#56 Barry Desborough

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Posted 20 September 2013 - 10:07 AM

Your comment that "None of this can be made any sense of by a 'designer' hypothesis" implies that you are "questioning the intention of the designer", n'est pas?

 

I don't need to supply the intention of the designer unless it can be pointed out that it actually IS the intention of the designer. 

No. I don't think anyone or anything designed ERVs. Retroviruses could have been designed, maybe by some super alien intelligence waging biological warfare, but it's a bit of a stretch, to say the least. And even if it was true, it would not affect the conclusion that ERVs are the inherited remnants of retroviral integrations into ancestral germ-lines.

 

I can't make any sense of your second sentence. Are you agreeing with me that ERVs are not designed?



#57 Salsa

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Posted 20 September 2013 - 10:32 AM

I'm saying that in a fallen world it is impossible to say exactly what the original design was.



#58 Adam Nagy

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Posted 20 September 2013 - 10:51 AM


I'm saying that in a fallen world it is impossible to say exactly what the original design was.

Barry is not exhibiting any form of interest in a dialogue. Why should he? He knows it all ;)

#59 Barry Desborough

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Posted 20 September 2013 - 11:02 AM

I'm saying that in a fallen world it is impossible to say exactly what the original design was.

“I do not feel obliged to believe that the same God who has endowed us with sense, reason, and intellect has intended us to forgo their use.” - Galileo Galilei, Letter to the Grand Duchess Christina



#60 Barry Desborough

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Posted 20 September 2013 - 11:07 AM

Barry is not exhibiting any form of interest in a dialogue. Why should he? He knows it all wink.png 

How do you have a dialogue with someone who does not believe you can have any confidence whatsoever in any notions at all?






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