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Re: More information

That quote refers to specific species. If you find one that shows that all species have these same hotspots, then let us know. But showing specific species hotspots only increases your problem, as this makes it even more unlikely taht they will all conect to the same location, because different species have differet hotspots for retrovirus hosting.

BTW, most of these quotes, if you pay attention, support evolution. :)

--- --- --- --- --- --- --- --- ---

Replying to:

“In each one of these studies, the presence or absence of a repetitive element at a specific locus in a given species was determined experimentally by PCR analysis, using flanking sequences as primers. It has been suggested that such experimental studies would not make a widespread contribution to phylogenetic inference in the short term, because the time, money, and effort needed to collect data on relatively few characters would be prohibitive (Hillis 1999) …
For example, in their analysis of Alu elements to determine Primate phylogeny, Salem et al. (2003) identified seven loci with an Alu element clearly present in human and chimp genomes and clearly absent from gorilla, and one locus with an Alu element clearly present in human and gorilla and clearly absent from chimp; they concluded that the contradictory locus was due to incomplete lineage sorting: the Alu element at that locus was polymorphic at the time of divergence of gorilla from human and chimp, remained polymorphic at the time of divergence of chimp from human, and eventually became fixed in human and gorilla lineages but not in chimp. Incomplete lineage sorting and the incompatible loci they create can complicate any phylogenetic analysis, but generally should not pose a problem in phylogenetic analyses using repetitive elements, as long as a sufficiently large number of independent loci are examined (Shedlock and Okada 2000).
In an automated analysis of thousands of repeats, rare instances of insertion homoplasy may also appear. According to Shedlock and Okada (2000), SINEs and LINEs are predominantly homoplasy-free, but hotspots of insertion may occur in exceptional cases. Indeed, Cantrell et al. (2001) have identified a locus containing two such hotspots, leading to SINE insertion homoplasy in multiple rodent species. We have found evidence of insertion homoplasy in our own data set: Figure 3 illustrates that a strong alignment appears to exist for a SINE repeat in cat and rat, while the absence of this repeat is strongly supported in baboon, cat, dog, cow, pig, and mouse, implying a phylogeny that is almost certainly incorrect. This repeat that is shared by cat and rat in an orthologous location is not an error, but accurately reflects the actual sequence data. Incomplete lineage sorting does not seem to be a plausible explanation for this example, as polymorphism of the presence or absence of the repeat would need to persist from the time of divergence of Rodents and Laurasiatheria (cat, dog, cow, pig) through the time of divergence of cat and dog, which seems unlikely. We speculate instead that this may be a rare instance of insertion homoplasy…
The (rare) presence of repeats that are incompatible with the correct phylogeny leads to two questions. First, how can we determine the correct phylogeny in the presence of conflicting evidence? Second, given a set of orthologous repeats that are incompatible with the correct phylogeny, how can we determine if these are instances of insertion homoplasy, incomplete lineage sorting, or erroneous alignment? …
“Orthologous repeats and mammalian phylogenetic inference”
http://www.genome.org/cgi/content/full/15/7/998

Re: Retroviruses

1. So let me get this straight. In order to explain why they got there, we must explain how they evolved? Once again you raise the bar. Next for chromsome #2 you'll ask us to explain the step-by step scenario, giving examples of every gene, allowing for the evolution of the first living thing to chimp. You ask for unreasonable tasks and think that you're proving something. Now stop avoiding the question and explain how they fit into creationism.

Also, the origin of life ISN'T evolution. Check the index to creationists claims on Talk Origins. They say outright taht they are seperate. You simply lied by saying that Talk Origins says the exact opposite.

2. YOu're kidding, right?
http://en.wikipedia.org/wiki/Retroviruses

You couldn't do this on your own? BTW, almost every single dormant ERV does NOTHING. That's what makes them such a problem for creationism.

3. They wouldn't. They would be filtered out, or would kill the organism. But dormant ERVs, like the 100,000 within our own genome, do nothing. They would be preserved. It just takes a population to breed as they usually do to spread these.

4. These are viruses. The species range for them is small. For them to infect every species on the planet is impossible unless they were at some point on species. Also, their location is random. The only logical explanation for them all being in the same place is that they are descendants from the organism which was originally infected.

That quote made no point whatsoever. That article is about the evolution of WHALES.

Second quote: yay. You found one portion of DNA more susceptible to ERVs than others. That still doesn't help your case. we're talking VIRUSES. Show me just ONE viruse capable of infecting every species on the planet. One taht is genetically capable. There is no such thing. Show me ONE that ALWAYS latches on to the same place. Not one that goes to one location more than others. One that ALWAYS does it. Because taht is what we see in nature. Once again, there is not one that does so. Also, those are hotspots in WHALES (Thats what the article is about, afterall). Not all organisms share these same hotspots. And yet tehy all share ERVs in the same location, and the degree at which they share them fits evolutionary expectations to a T.

Next quote: Perhaps you missed this paragraph directly underneath the one you quoted.
"On the other hand, the combining of molecular biological methodologies with those of bioinformatics in the analysis of retroposed elements provides a reliable, homoplasy-free reconstruction of phylogenetic trees. In this study, we have unambiguously substantiated the monophyly of the placental, boreotherian, supraprimates, and laurasiatherian mammalian clades with multiple pieces of independent evidence from retroposon presence/absence data. Furthermore, by screening nearly 21 million genomic trace sequences we found two retropositions that lend support to the Epitheria hypothesis [ 13]. Interestingly, this is an area where sequence-based tree analyses have tended to support other trees, but at least some authors have remained skeptical of the ability of automatic tree-building procedures to infer the root of the mammalian tree when all data are known to violate the underlying model of sequence evolution [ 1, 4, 5, 10, 12]."

How strange that you miss that one.

--- --- --- --- --- --- --- --- ---

Replying to:

This is in response to:

"2. ERVs. YOu never did reply to them when Kabane52 presented them to you."
http://pub17.bravenet.com/forum/1424646898/fetch/729592/2

Because evolutionists claim that Retroviruses are proof for common descent, please answer these questions to prove they actually are:

1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus.
(Refer to http://en.wikipedia.org/wiki/Virus for reference and in case you didn’t know that “The origins of modern viruses are not entirely clear.”)
Don’t bother arguing that this is NOT part of evolution, but rather the separate science of Abiogenesis. Viruses were obviously created after ‘something’ miraculously created life and, as seen on the Berkeley/ NSCE and TalkOrigins websites (to name just a few), the origin of life is still part of evolution - no matter how evolutionists would like to rewrite their history.
http://evolution.berkeley.edu/evolibrary/article/0_0_0/origsoflife_04 http://www.talkorigins.org/faqs/abioprob/

2. Explain in detail the PROVEN positive and negative effects of retroviruses on their hosts.

3. Explain in detail why harmful retroviruses would be preserved by positive selection.

4. Explain in detail why you think that insertion bias for certain loci indicate common descent .

“ In their recent assessment of morphological and molecular evidence for inferring cetacean ancestry, Luckett and Hong (1998) badly misconstrue how SINEs evolved, misinterpret how they are used for phylogeny inference, and incorrectly dismiss evidence from SINEs that conclusively demonstrate paraphyly of the Artiodactyla …
In conclusion, confusion between the statistical nature of inferring phylogeny from DNA sequences and constructing cladograms based on SINE insertion analysis can lead to dangerous generalizations in the literature about the unreliability of molecular data …”
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us


“We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.”
“An ancient retrovirus-like element contains hot spots for SINE insertion.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1461688

“Recently, Bashir et al. [ 44] published a purely computational method for reconstructing the phylogenetic relationships between mammals by automatically scanning for the presence and/or absence of transposed elements in mammalian sequences. However, this use of pure bioinformatics is fraught with pitfalls. The available sequence information is often not reliable, sequence drift makes identifying orthologous insertions extremely difficult, and full sequences are available for only a limited number of species. Extreme care must be taken to conclusively verify that supposedly homoplasmic insertions belong to the same class of transposons and are integrated at orthologous positions. For high-quality, reliable phylogenetic inferences it is essential to individually characterize the nature of each insertion as well as its integration site, a process not amenable to high-throughput computational searches and incomplete species sampling. “
“Retroposed Elements as Archives for the Evolutionary History of Placental Mammals”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1395351

Did I miss your proof?

1. Since it's your claim, the burden of proof it yours.

2. If I missed your proof in your postings, let me know.

3. Are you throwing in the towel by changing the topic to chromosome #2? I recommend we finish this up before going on ...

I will follow-up tomorrow regarding your claim of dormant ERVs doing nothing, but I'll give you a chance to retract your comment if you wish...

--- --- --- --- --- --- --- --- ---

Replying to:

1. So let me get this straight. In order to explain why they got there, we must explain how they evolved? Once again you raise the bar. Next for chromsome #2 you'll ask us to explain the step-by step scenario, giving examples of every gene, allowing for the evolution of the first living thing to chimp. You ask for unreasonable tasks and think that you're proving something. Now stop avoiding the question and explain how they fit into creationism.

Also, the origin of life ISN'T evolution. Check the index to creationists claims on Talk Origins. They say outright taht they are seperate. You simply lied by saying that Talk Origins says the exact opposite.

2. YOu're kidding, right?
http://en.wikipedia.org/wiki/Retroviruses

You couldn't do this on your own? BTW, almost every single dormant ERV does NOTHING. That's what makes them such a problem for creationism.

3. They wouldn't. They would be filtered out, or would kill the organism. But dormant ERVs, like the 100,000 within our own genome, do nothing. They would be preserved. It just takes a population to breed as they usually do to spread these.

4. These are viruses. The species range for them is small. For them to infect every species on the planet is impossible unless they were at some point on species. Also, their location is random. The only logical explanation for them all being in the same place is that they are descendants from the organism which was originally infected.

That quote made no point whatsoever. That article is about the evolution of WHALES.

Second quote: yay. You found one portion of DNA more susceptible to ERVs than others. That still doesn't help your case. we're talking VIRUSES. Show me just ONE viruse capable of infecting every species on the planet. One taht is genetically capable. There is no such thing. Show me ONE that ALWAYS latches on to the same place. Not one that goes to one location more than others. One that ALWAYS does it. Because taht is what we see in nature. Once again, there is not one that does so. Also, those are hotspots in WHALES (Thats what the article is about, afterall). Not all organisms share these same hotspots. And yet tehy all share ERVs in the same location, and the degree at which they share them fits evolutionary expectations to a T.

Next quote: Perhaps you missed this paragraph directly underneath the one you quoted.
"On the other hand, the combining of molecular biological methodologies with those of bioinformatics in the analysis of retroposed elements provides a reliable, homoplasy-free reconstruction of phylogenetic trees. In this study, we have unambiguously substantiated the monophyly of the placental, boreotherian, supraprimates, and laurasiatherian mammalian clades with multiple pieces of independent evidence from retroposon presence/absence data. Furthermore, by screening nearly 21 million genomic trace sequences we found two retropositions that lend support to the Epitheria hypothesis [ 13]. Interestingly, this is an area where sequence-based tree analyses have tended to support other trees, but at least some authors have remained skeptical of the ability of automatic tree-building procedures to infer the root of the mammalian tree when all data are known to violate the underlying model of sequence evolution [ 1, 4, 5, 10, 12]."

How strange that you miss that one.

--- --- --- --- --- --- --- --- ---

Replying to:

This is in response to:

"2. ERVs. YOu never did reply to them when Kabane52 presented them to you."
http://pub17.bravenet.com/forum/1424646898/fetch/729592/2

Because evolutionists claim that Retroviruses are proof for common descent, please answer these questions to prove they actually are:

1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus.
(Refer to http://en.wikipedia.org/wiki/Virus for reference and in case you didn’t know that “The origins of modern viruses are not entirely clear.”)
Don’t bother arguing that this is NOT part of evolution, but rather the separate science of Abiogenesis. Viruses were obviously created after ‘something’ miraculously created life and, as seen on the Berkeley/ NSCE and TalkOrigins websites (to name just a few), the origin of life is still part of evolution - no matter how evolutionists would like to rewrite their history.
http://evolution.berkeley.edu/evolibrary/article/0_0_0/origsoflife_04 http://www.talkorigins.org/faqs/abioprob/

2. Explain in detail the PROVEN positive and negative effects of retroviruses on their hosts.

3. Explain in detail why harmful retroviruses would be preserved by positive selection.

4. Explain in detail why you think that insertion bias for certain loci indicate common descent .

“ In their recent assessment of morphological and molecular evidence for inferring cetacean ancestry, Luckett and Hong (1998) badly misconstrue how SINEs evolved, misinterpret how they are used for phylogeny inference, and incorrectly dismiss evidence from SINEs that conclusively demonstrate paraphyly of the Artiodactyla …
In conclusion, confusion between the statistical nature of inferring phylogeny from DNA sequences and constructing cladograms based on SINE insertion analysis can lead to dangerous generalizations in the literature about the unreliability of molecular data …”
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us


“We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.”
“An ancient retrovirus-like element contains hot spots for SINE insertion.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1461688

“Recently, Bashir et al. [ 44] published a purely computational method for reconstructing the phylogenetic relationships between mammals by automatically scanning for the presence and/or absence of transposed elements in mammalian sequences. However, this use of pure bioinformatics is fraught with pitfalls. The available sequence information is often not reliable, sequence drift makes identifying orthologous insertions extremely difficult, and full sequences are available for only a limited number of species. Extreme care must be taken to conclusively verify that supposedly homoplasmic insertions belong to the same class of transposons and are integrated at orthologous positions. For high-quality, reliable phylogenetic inferences it is essential to individually characterize the nature of each insertion as well as its integration site, a process not amenable to high-throughput computational searches and incomplete species sampling. “
“Retroposed Elements as Archives for the Evolutionary History of Placental Mammals”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1395351

Re: Did I miss your proof?

1. That's just it. The origin of all viruses has nothing to do with my claim. You just raised the bar to an unreasonable level.
2. I explained how these are proof of common ancestry. You did miss it. Now, explain to my how these fit with creationism.
3. No. I was just tossing that in because it was another point you dodged before, and seem to be dodging now.

Well, almost all do nothing. A few have a function. A few in sheep are necessary for reproduction. However, I explain how this proves nothing in my ERV thread.

--- --- --- --- --- --- --- --- ---

Replying to:

1. Since it's your claim, the burden of proof it yours.

2. If I missed your proof in your postings, let me know.

3. Are you throwing in the towel by changing the topic to chromosome #2? I recommend we finish this up before going on ...

I will follow-up tomorrow regarding your claim of dormant ERVs doing nothing, but I'll give you a chance to retract your comment if you wish...

--- --- --- --- --- --- --- --- ---

Replying to:

1. So let me get this straight. In order to explain why they got there, we must explain how they evolved? Once again you raise the bar. Next for chromsome #2 you'll ask us to explain the step-by step scenario, giving examples of every gene, allowing for the evolution of the first living thing to chimp. You ask for unreasonable tasks and think that you're proving something. Now stop avoiding the question and explain how they fit into creationism.

Also, the origin of life ISN'T evolution. Check the index to creationists claims on Talk Origins. They say outright taht they are seperate. You simply lied by saying that Talk Origins says the exact opposite.

2. YOu're kidding, right?
http://en.wikipedia.org/wiki/Retroviruses

You couldn't do this on your own? BTW, almost every single dormant ERV does NOTHING. That's what makes them such a problem for creationism.

3. They wouldn't. They would be filtered out, or would kill the organism. But dormant ERVs, like the 100,000 within our own genome, do nothing. They would be preserved. It just takes a population to breed as they usually do to spread these.

4. These are viruses. The species range for them is small. For them to infect every species on the planet is impossible unless they were at some point on species. Also, their location is random. The only logical explanation for them all being in the same place is that they are descendants from the organism which was originally infected.

That quote made no point whatsoever. That article is about the evolution of WHALES.

Second quote: yay. You found one portion of DNA more susceptible to ERVs than others. That still doesn't help your case. we're talking VIRUSES. Show me just ONE viruse capable of infecting every species on the planet. One taht is genetically capable. There is no such thing. Show me ONE that ALWAYS latches on to the same place. Not one that goes to one location more than others. One that ALWAYS does it. Because taht is what we see in nature. Once again, there is not one that does so. Also, those are hotspots in WHALES (Thats what the article is about, afterall). Not all organisms share these same hotspots. And yet tehy all share ERVs in the same location, and the degree at which they share them fits evolutionary expectations to a T.

Next quote: Perhaps you missed this paragraph directly underneath the one you quoted.
"On the other hand, the combining of molecular biological methodologies with those of bioinformatics in the analysis of retroposed elements provides a reliable, homoplasy-free reconstruction of phylogenetic trees. In this study, we have unambiguously substantiated the monophyly of the placental, boreotherian, supraprimates, and laurasiatherian mammalian clades with multiple pieces of independent evidence from retroposon presence/absence data. Furthermore, by screening nearly 21 million genomic trace sequences we found two retropositions that lend support to the Epitheria hypothesis [ 13]. Interestingly, this is an area where sequence-based tree analyses have tended to support other trees, but at least some authors have remained skeptical of the ability of automatic tree-building procedures to infer the root of the mammalian tree when all data are known to violate the underlying model of sequence evolution [ 1, 4, 5, 10, 12]."

How strange that you miss that one.

--- --- --- --- --- --- --- --- ---

Replying to:

This is in response to:

"2. ERVs. YOu never did reply to them when Kabane52 presented them to you."
http://pub17.bravenet.com/forum/1424646898/fetch/729592/2

Because evolutionists claim that Retroviruses are proof for common descent, please answer these questions to prove they actually are:

1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus.
(Refer to http://en.wikipedia.org/wiki/Virus for reference and in case you didn’t know that “The origins of modern viruses are not entirely clear.”)
Don’t bother arguing that this is NOT part of evolution, but rather the separate science of Abiogenesis. Viruses were obviously created after ‘something’ miraculously created life and, as seen on the Berkeley/ NSCE and TalkOrigins websites (to name just a few), the origin of life is still part of evolution - no matter how evolutionists would like to rewrite their history.
http://evolution.berkeley.edu/evolibrary/article/0_0_0/origsoflife_04 http://www.talkorigins.org/faqs/abioprob/

2. Explain in detail the PROVEN positive and negative effects of retroviruses on their hosts.

3. Explain in detail why harmful retroviruses would be preserved by positive selection.

4. Explain in detail why you think that insertion bias for certain loci indicate common descent .

“ In their recent assessment of morphological and molecular evidence for inferring cetacean ancestry, Luckett and Hong (1998) badly misconstrue how SINEs evolved, misinterpret how they are used for phylogeny inference, and incorrectly dismiss evidence from SINEs that conclusively demonstrate paraphyly of the Artiodactyla …
In conclusion, confusion between the statistical nature of inferring phylogeny from DNA sequences and constructing cladograms based on SINE insertion analysis can lead to dangerous generalizations in the literature about the unreliability of molecular data …”
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us


“We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.”
“An ancient retrovirus-like element contains hot spots for SINE insertion.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1461688

“Recently, Bashir et al. [ 44] published a purely computational method for reconstructing the phylogenetic relationships between mammals by automatically scanning for the presence and/or absence of transposed elements in mammalian sequences. However, this use of pure bioinformatics is fraught with pitfalls. The available sequence information is often not reliable, sequence drift makes identifying orthologous insertions extremely difficult, and full sequences are available for only a limited number of species. Extreme care must be taken to conclusively verify that supposedly homoplasmic insertions belong to the same class of transposons and are integrated at orthologous positions. For high-quality, reliable phylogenetic inferences it is essential to individually characterize the nature of each insertion as well as its integration site, a process not amenable to high-throughput computational searches and incomplete species sampling. “
“Retroposed Elements as Archives for the Evolutionary History of Placental Mammals”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1395351

Re: Did I miss your proof?

I'd like to take my possibly last chance and point out the irony in #1.

1. You say that, but when it comes to your genetic barriers, it's the other way around. You say it's there, but we have to prove it isn't.

--- --- --- --- --- --- --- --- ---

Replying to:

1. Since it's your claim, the burden of proof it yours.

2. If I missed your proof in your postings, let me know.

3. Are you throwing in the towel by changing the topic to chromosome #2? I recommend we finish this up before going on ...

I will follow-up tomorrow regarding your claim of dormant ERVs doing nothing, but I'll give you a chance to retract your comment if you wish...

--- --- --- --- --- --- --- --- ---

Replying to:

1. So let me get this straight. In order to explain why they got there, we must explain how they evolved? Once again you raise the bar. Next for chromsome #2 you'll ask us to explain the step-by step scenario, giving examples of every gene, allowing for the evolution of the first living thing to chimp. You ask for unreasonable tasks and think that you're proving something. Now stop avoiding the question and explain how they fit into creationism.

Also, the origin of life ISN'T evolution. Check the index to creationists claims on Talk Origins. They say outright taht they are seperate. You simply lied by saying that Talk Origins says the exact opposite.

2. YOu're kidding, right?
http://en.wikipedia.org/wiki/Retroviruses

You couldn't do this on your own? BTW, almost every single dormant ERV does NOTHING. That's what makes them such a problem for creationism.

3. They wouldn't. They would be filtered out, or would kill the organism. But dormant ERVs, like the 100,000 within our own genome, do nothing. They would be preserved. It just takes a population to breed as they usually do to spread these.

4. These are viruses. The species range for them is small. For them to infect every species on the planet is impossible unless they were at some point on species. Also, their location is random. The only logical explanation for them all being in the same place is that they are descendants from the organism which was originally infected.

That quote made no point whatsoever. That article is about the evolution of WHALES.

Second quote: yay. You found one portion of DNA more susceptible to ERVs than others. That still doesn't help your case. we're talking VIRUSES. Show me just ONE viruse capable of infecting every species on the planet. One taht is genetically capable. There is no such thing. Show me ONE that ALWAYS latches on to the same place. Not one that goes to one location more than others. One that ALWAYS does it. Because taht is what we see in nature. Once again, there is not one that does so. Also, those are hotspots in WHALES (Thats what the article is about, afterall). Not all organisms share these same hotspots. And yet tehy all share ERVs in the same location, and the degree at which they share them fits evolutionary expectations to a T.

Next quote: Perhaps you missed this paragraph directly underneath the one you quoted.
"On the other hand, the combining of molecular biological methodologies with those of bioinformatics in the analysis of retroposed elements provides a reliable, homoplasy-free reconstruction of phylogenetic trees. In this study, we have unambiguously substantiated the monophyly of the placental, boreotherian, supraprimates, and laurasiatherian mammalian clades with multiple pieces of independent evidence from retroposon presence/absence data. Furthermore, by screening nearly 21 million genomic trace sequences we found two retropositions that lend support to the Epitheria hypothesis [ 13]. Interestingly, this is an area where sequence-based tree analyses have tended to support other trees, but at least some authors have remained skeptical of the ability of automatic tree-building procedures to infer the root of the mammalian tree when all data are known to violate the underlying model of sequence evolution [ 1, 4, 5, 10, 12]."

How strange that you miss that one.

--- --- --- --- --- --- --- --- ---

Replying to:

This is in response to:

"2. ERVs. YOu never did reply to them when Kabane52 presented them to you."
http://pub17.bravenet.com/forum/1424646898/fetch/729592/2

Because evolutionists claim that Retroviruses are proof for common descent, please answer these questions to prove they actually are:

1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus.
(Refer to http://en.wikipedia.org/wiki/Virus for reference and in case you didn’t know that “The origins of modern viruses are not entirely clear.”)
Don’t bother arguing that this is NOT part of evolution, but rather the separate science of Abiogenesis. Viruses were obviously created after ‘something’ miraculously created life and, as seen on the Berkeley/ NSCE and TalkOrigins websites (to name just a few), the origin of life is still part of evolution - no matter how evolutionists would like to rewrite their history.
http://evolution.berkeley.edu/evolibrary/article/0_0_0/origsoflife_04 http://www.talkorigins.org/faqs/abioprob/

2. Explain in detail the PROVEN positive and negative effects of retroviruses on their hosts.

3. Explain in detail why harmful retroviruses would be preserved by positive selection.

4. Explain in detail why you think that insertion bias for certain loci indicate common descent .

“ In their recent assessment of morphological and molecular evidence for inferring cetacean ancestry, Luckett and Hong (1998) badly misconstrue how SINEs evolved, misinterpret how they are used for phylogeny inference, and incorrectly dismiss evidence from SINEs that conclusively demonstrate paraphyly of the Artiodactyla …
In conclusion, confusion between the statistical nature of inferring phylogeny from DNA sequences and constructing cladograms based on SINE insertion analysis can lead to dangerous generalizations in the literature about the unreliability of molecular data …”
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us


“We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.”
“An ancient retrovirus-like element contains hot spots for SINE insertion.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1461688

“Recently, Bashir et al. [ 44] published a purely computational method for reconstructing the phylogenetic relationships between mammals by automatically scanning for the presence and/or absence of transposed elements in mammalian sequences. However, this use of pure bioinformatics is fraught with pitfalls. The available sequence information is often not reliable, sequence drift makes identifying orthologous insertions extremely difficult, and full sequences are available for only a limited number of species. Extreme care must be taken to conclusively verify that supposedly homoplasmic insertions belong to the same class of transposons and are integrated at orthologous positions. For high-quality, reliable phylogenetic inferences it is essential to individually characterize the nature of each insertion as well as its integration site, a process not amenable to high-throughput computational searches and incomplete species sampling. “
“Retroposed Elements as Archives for the Evolutionary History of Placental Mammals”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1395351

Probably, you deleted a bunch of posts...

As I pointed out. Your four questions attempting to move the goalposts on ERVs were not germane to the original subject. Of course, if I were trying to argue your position I would be desperate, too. ERVs are devastating to those who want to deny common ancestry. You have no answer other than to delete what you can't refute. So, I guess you agree.

WiYC, thanks for quoting Shedlock, Milinkovitch, and Okada

I like that article. It supports Thewissen on whale evolution. They were questioning Luckett and Hongs' criticism of the SINES supporting artyocactyl whale origin. You really ought to read the whole paper and the one they reference before quoting.

"Recent and extensive phylogenetic re-analyses (Gatesy et al., 1999) of all available data indicate that the inclusio of a momphyletic Cetacea within the phylogenetic tree of Artiodactyla has been stable to increased taxomic sampling and to the addition of nearly nine thousand characters (of which over 1,500 are pasimony-informative) from three mtDNA genes, 12 nuclear genes and eight SINE retroposon loci (Fig. 1). Although the concepts of ceatceans as highly derived artiodactyls stil raises major scepticism(e.g. Luckett and Hong, 1998, Heyning, 1999), it constitutes one of the best supported hypotheses of interordinal (sensu lato) relationship wit in the phoylogeny of mammals."

Marine Mammals: Biology and Conservation by Peter G. H. Evans, Juan Antonio Raga p. 327

The SINE evidence is pretty strong on its own considering they have eight separate insertions. When you couple that with better fossil evidence (astragali) and earlier protein evidence it is game over. The problem for creationists is that these genetic tools are just getting better and they keep confirming evolution.

Peromyscus?

WiYC quotes:
“We have identified two hot spots for SINE insertion within mys-9 and at each hot spot have found that two independent SINE insertions have occurred at identical sites. These results have major repercussions for phylogenetic analyses based on SINE insertions, indicating the need for caution when one concludes that the existence of a SINE at a specific locus in multiple individuals is indicative of common ancestry. Although independent insertions at the same locus may be rare, SINE insertions are not homoplasy-free phylogenetic markers.”
“An ancient retrovirus-like element contains hot spots for SINE insertion.”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1461688

I don't think that anyone has brought up a case for common ancestry bases solely on a SINGLE SINE at A SPECIFIC locus. In the whale instance, we have eight SINES in the chimp/human we have eight (so far). Homoplasy would be extremely unlikely in a single instance. The odds against it with seven or eight SINES is atronomical. Besides, who was talking about deer mice.

Read the paper. This is science providing new tools to refine our understanding.

WiYC quoted Kriegs, Churakov, Kiefmann, Brosius and Schmitz:

“Recently, Bashir et al. [ 44] published a purely computational method for reconstructing the phylogenetic relationships between mammals by automatically scanning for the presence and/or absence of transposed elements in mammalian sequences. However, this use of pure bioinformatics is fraught with pitfalls. The available sequence information is often not reliable, sequence drift makes identifying orthologous insertions extremely difficult, and full sequences are available for only a limited number of species. Extreme care must be taken to conclusively verify that supposedly homoplasmic insertions belong to the same class of transposons and are integrated at orthologous positions. For high-quality, reliable phylogenetic inferences it is essential to individually characterize the nature of each insertion as well as its integration site, a process not amenable to high-throughput computational searches and incomplete species sampling. “
“Retroposed Elements as Archives for the Evolutionary History of Placental Mammals”
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1395351

Yes, there are short-comings to the application of some methods in some circumstances as the quotation states. However, the caution to use care does not mean using SINES are useless. Note that they criticize the method used in another study and offer a way to better analyze phylogeny. At the same time, the paper acknowleges that analyzing relationships on the basis of molecular sampling has corrected earlier cladistic misgroupings based on morphology.

"Reconstruction of the placental mammalian (eutherian) evolutionary tree has undergone diverse revisions, and numerous aspects remain hotly debated. Initial hierarchical divisions based on morphology contained many misgroupings due to features that evolved independently by similar selection processes. Molecular analyses corrected many of these misgroupings and the superordinal hierarchy of placental mammals was recently assembled into four clades."

Science becomes more powerful as alternative tools and methods are developed to test conclusions. This team is using retrotransposons to test relationships between mammal species. There strategies and refinements will strengthen this kind of analysis. This paper doesn't undermine the use of genetic markers to analyze phylogeny, it supports it. As there paper said discussing retroposed elements.

"Retroposed elements provide an exceptionally informative source of rare genomic changes. They are a virtually ambiguity-free approximation of evolutionary history [ 24, 25]. The nearly homoplasy-free character and innate complexity of retroposed elements in mammalian species, coupled with their high abundance, enables phylogenetic reconstructions based on a variety of alternative markers."

Moving the goalposts when you can't respond to ERV evidence for evolution

WiYC said:
"1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus."

The question at hand was whether or not you could respond to the evidence for evolution that is provided by ERVs. This has nothing to do with that. You obviously can't respond.

How retroviruses evolved billions of years ago does not change the fact that genetic evidence shows that they did infect the common ancestors of all great apes (including us) a few million years ago.

Re: Moving the goalposts when you can't respond to ERV evidence for evolution

For feather thread:

Will you stop deleting my links to articles already! Deleting them doesn't make them non-existant!

1. I said no such thing. I said that there is too much that we do not know about genes.

2. Here are the links to articles you continue to delete on teh subject of feather evolution.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WX0-4N3GFRW-1&_user=5908723&_coverDate=04%2F30%2F2007&_alid=621592783&_rdoc=2&_fmt=summary&_orig=search&_cdi=7144&_sort=d&_docanchor=&view=c&_ct=41&_acct=C000050221&_version=1&_urlVersion=0&_userid=5908723&md5=66c0d86bf513d97494a0bd402ca30539
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WDG-4N2KTJD-5&_user=5908723&_coverDate=05%2F01%2F2007&_alid=621592783&_rdoc=1&_fmt=summary&_orig=search&_cdi=6766&_sort=d&_docanchor=&view=c&_ct=41&_acct=C000050221&_version=1&_urlVersion=0&_userid=5908723&md5=79a81a12564e8c8a534426c17693d492
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VRW-4M4KK5D-1&_user=5908723&_coverDate=12%2F31%2F2006&_alid=621592783&_rdoc=3&_fmt=summary&_orig=search&_cdi=6245&_sort=d&_docanchor=&view=c&_ct=41&_acct=C000050221&_version=1&_urlVersion=0&_userid=5908723&md5=6930394eb57ddf3bf04d3ec604921ccd

Now either acknowledge that they exist or stoip acting high and mighty.

Goalpost argument

In regard to your comment:

"WiYC said:
"1. Explain in detail a hypothetical genetic step-by-step scenario of the evolution of the first virus."

The question at hand was whether or not you could respond to the evidence for evolution that is provided by ERVs. This has nothing to do with that. You obviously can't respond."


Discussing how and why viruses ‘evolved’ (retroviruses in particular) in addition to the continued evolution of viruses is critical to the argument:

"Clearly, properly understanding the nature of SINE retroposons and how they evolve is fundamental to their intelligent application as phylogenetic tools."
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us


2. In regard to your comment:

"How retroviruses evolved billions of years ago does not change the fact that genetic evidence shows that they did infect the common ancestors of all great apes (including us) a few million years ago."


Retrovirus 'infection' does NOT prove common descent.

Please provide your 'genetic evidence.'

You need to understand what they are talking about.

WiYC:
Discussing how and why viruses ‘evolved’ (retroviruses in particular) in addition to the continued evolution of viruses is critical to the argument:

"Clearly, properly understanding the nature of SINE retroposons and how they evolve is fundamental to their intelligent application as phylogenetic tools."
“SINE Evolution, Missing Data, and the Origin of Whales”
http://209.85.165.104/search?q=cache:O7yDdmkPl1cJ:www.ulb.ac.be/sciences/ueg/pdf_files/shedlock%26al_00.pdf+hillis+9980+sine+evolution&hl=en&ct=clnk&cd=1&gl=us

You really should read the article. They are talking about changes in SINES not retroviruses. SINES are the remnants of an earlier infection. If you read the section just after what is quoted, they explain how SINES are effected by subsiquent evolution of the host.

If you would actually read what I posted about your questions and the links I provided, you would understand this issue. From the very article you quote, the authors support the use of SINES to establish artyodactyl descent for whales. They criticize the Lucket and Hong for not understanding how SINES evolve.

"In there recent assessment of morphological and molecular evidence for inferring cetacean ancestry, Luckett and Hong (1998) badly miscontrue how SINEs evolve, misinterpret how they are used for phylogeny inference, and incorrectly dismiss evidence from SINEs that conclusively demonstrate paraphyly of the Artiodacyla. We believe this is a serious problem that is counterproductive to advancing an accurate understanding of cetacean evolution and unfortunately promotes a negative view regarding the value of molecular data that goes well beyond the current debate about whale origins."

Note that the paper talks about the evolution of SINEs (Short Interspersed Elements) are not retroviruses. Although they are one of the four classes of retrotransposons. SINE insertions are also evidence of common descent. They are much shorter segments of code than ERVs. "These are approximately 300 bp long and do not encode any protein sequence. The recent DNA sequence analysis of the human genome found about 1.1 million Alus, comprising 10.6% of the DNA (Nature 409:860, 2001)."
http://www.talkorigins.org/faqs/molgen/

ERVs are much longer and more complex. They were noted after intensive studies retroviruses because they are structured like them.

"Soon after the discovery of infections retroviruses, scientists noticed that similar sequences were present in the DNA of many mammalian species, including humans; these copies are called endogenous retroviruses, and presumably represent the consequences of ancient retroviral infections of germline cells. In human DNA there are about 8 different classes of endogenous retroviruses with members of each class varying in number from one or two to more than 50 copies. Essentially all of these endogenous retroviruses contain mutations that would disrupt the function of their genes, as would be expected if they inserted millions of years ago with no selective pressure to maintain the function of the genes. In addition, the duplicated LTR sequences represent potential targets for "homologous recombination" events that delete the DNA between the corresponding region of the LTRs, leaving only a single composite LTR sequence; many more copies of these isolated LTR fragments exist in the DNA than complete retroviral copies."
http://www.talkorigins.org/faqs/molgen/

ERVs are no longer active viruses either. They have become artifacts in the DNA of the host species. To conclude, understanding how SINEs or ERVs evolve within the host is indeed important to understanding how to use them to determine phylogenetic sequences. However, neither would require an understanding of the origin of retroviruses. SINEs never were viruses and ERVs are no longer active viruses. Both do evolve within the host, but because neither are functional there is no selective pressure which allows them to continue to change. This is why ERVs are so effective for determining phylogeny.

First you deleted the post providing evidence for ERVs supporting common descent.

WiYC said:
"Retrovirus 'infection' does NOT prove common descent.

Please provide your 'genetic evidence.'"

I provided the evidence in an earlier post addressing one of your four questions.