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

[Split Rock]

That is evidence I accept. There is no other.

I see that dad is still arrogant and self-absorbed. Tell us something, dad... how does one "occupy science?"

 

[Naraoia]

"Given the size of vertebrate genomes (>1 × 109 bp)...

A superscript was lost in copy-paste.

 

[dad]

I see that dad is still arrogant and self-absorbed. Tell us something, dad... how does one "occupy science?"

Think of it as an intellectual tent. In it is a con artist called so called science. Well, we simply tell the cad to get out, and occupy the tent with truth.

 

[cupid dave]

Think of it as an intellectual tent. In it is a con artist called so called science. Well, we simply tell the cad to get out, and occupy the tent with truth.

Paradigm.

The right word is that Science is the paradigm for the way we now look at Nature and Truth.

It is merely the current perspective on what is Fact and what is unsupported ideas.

In the science paradigm of the Middle Ages, the sun went around the earth.
Everyone accepted that paradigm, because arguments established the view over other ideas.

Even the Bible people used that view in trying to make sense out of Genesis.

 

[dad]

Paradigm.

The right word is that Science is the paradigm for the way we now look at Nature and Truth.

It is merely the current perspective on what is Fact and what is unsupported ideas.

In the science paradigm of the Middle Ages, the sun went around the earth.
Everyone accepted that paradigm, because arguments established the view over other ideas.

Even the Bible people used that view in trying to make sense out of Genesis.

Sounds good to me. 'Science is the way man looks at nature'! Opinion, in other words. 'Hey Joe, how is it fashionable to look at nature and truth this year-oh and is using the word paradigm still cool'?

The thing is that the nature they look at is present nature. Unless that nature extended and could be solidly evidenced to extend into the far past, we are looking at a fishbowl paradigm.

 

[Zaius137]

“So how did these authors determine if the same ERV’ was at the same location in the genome of humans and chimps? They didn't use genetic algorithms. They used PCR.”

I suppose you mean orthologous. Actually out of the tens of thousands of supposed ERV insertion in humans about 12 are shared with the apes and were located by algorithms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1054887/

http://www.talkorigins.org/faqs/comdesc/section4.html

A quick side point I would like to make…

Since there are literally tens of thousands of these insertions that must be fixed into the human population lets look at how long that would take according to Haldane and his 300T generations. In humans with about 20 years per generation and 300 generations that gives about 6000 years per single insertion. Now a conservative estimate of 10 thousand insertion sites gives 10k times 6k which equals about 60 million years between the common ancestor of apes and humans. That figure is ten times the supposed divergence time.

Can there be another explanation other than common ancestry. Of course there is; what if the loci of these insertions were highly selective and independent events in humans and apes.

“But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to280 times more frequently than predicted mathematically.”

http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

Are ERV’s an indication of common decent or common design.

 

[Astridhere]

“So how did these authors determine if the same ERV’ was at the same location in the genome of humans and chimps? They didn't use genetic algorithms. They used PCR.”

I suppose you mean orthologous. Actually out of the tens of thousands of supposed ERV insertion in humans about 12 are shared with the apes and were located by algorithms.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1054887/

http://www.talkorigins.org/faqs/comdesc/section4.html

A quick side point I would like to make…

Since there are literally tens of thousands of these insertions that must be fixed into the human population lets look at how long that would take according to Haldane and his 300T generations. In humans with about 20 years per generation and 300 generations that gives about 6000 years per single insertion. Now a conservative estimate of 10 thousand insertion sites gives 10k times 6k which equals about 60 million years between the common ancestor of apes and humans. That figure is ten times the supposed divergence time.

Can there be another explanation other than common ancestry. Of course there is; what if the loci of these insertions were highly selective and independent events in humans and apes.

“But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to280 times more frequently than predicted mathematically.”

http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

Are ERV’s an indication of common decent or common design.

What I like most of all is evolutionists inability to deal with the non credibility of algorithms that do no more than chase ghosts, ignore dissimilarity, never add up without bottlenecks and provides data that changes like the wind.

Let's see what flavour of the month ensues as a response to you.

Indeed, it will be another poor response and attempt to pass this nonsense off as science.

 

[Naraoia]

I suppose you mean orthologous. Actually out of the tens of thousands of supposed ERV insertion in humans about 12 are shared with the apes and were located by algorithms.
Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans

That paper specifically looked at a class of ERVs that was not shared between humans and other apes. I assume you refer to this paragraph:

Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3). We classified these as “ambiguous” overlap loci (Figure 3). If all 24 locations corresponded to insertions that were orthologous for each pair, this would correspond to a maximum of 12 orthologous loci. The number of non-orthologous loci was calculated as 275/287 (275 + 12) or 95.8%. This is almost certainly a lower-bound estimate owing to the limitation of our BAC-based mapping approach to refine the precise locations of the insertions.

Please read the paragraph before this one carefully. They are talking about a comparison of chimps, gorillas, macaques and baboons. The human genome was used as a reference to map the sequences around the actual ERVs, it was not part of the comparison proper. Remember, PTERV1 insertions are absent from the human genome, so human PTERV1 insertions cannot be orthologous to anything. Because they don't exist.

Basically, it's their way of determining whether the insertions were orthologous in chimps, gorillas, macaques and baboons. Sequence a bit of the genomic neighbourhood of each insertion, map each to the human genome, and if two insertions in two different species map to the same region, they might be orthologous.

29+ Evidences for Macroevolution: Part 4

What the TalkOrigins article has to do with the above is a mystery. The section on ERVs looks like it hasn't even been updated since the human genome came out:

There are at least seven different known instances of common retrogene insertions between chimps and humans, and this number is sure to grow as both these organism's genomes are sequenced.

A quick side point I would like to make…

Since there are literally tens of thousands of these insertions that must be fixed into the human population lets look at how long that would take according to Haldane and his 300T generations. In humans with about 20 years per generation and 300 generations that gives about 6000 years per single insertion. Now a conservative estimate of 10 thousand insertion sites gives 10k times 6k which equals about 60 million years between the common ancestor of apes and humans. That figure is ten times the supposed divergence time.

If only one ERV is allowed to undergo fixation at a time, which is bullcrap. Just how many polymorphisms exist in the human gene pool right now? You seem to have a persistent problem with parallel vs. sequential trials.

Can there be another explanation other than common ancestry. Of course there is; what if the loci of these insertions were highly selective and independent events in humans and apes.

If you go back a few pages, I think Loudmouth posted evidence that retroviral insertions are pretty much random. They do have site preferences, but there are astronomical numbers of suitable sites in the genome.

“But although this concept of retrovirus selectivity is currently prevailing, practically all genomic regions were reported to be used as primary integration targets, however, with different preferences. There were identified 'hot spots' containing integration sites used up to 280 times more frequently than predicted mathematically.

I think "up to" 280 times is a lot less than you need to kick this particular p-value into non-significance...

 

[cupid dave]

When you have eliminated the impossible, (Gods) whatever remains, however improbable, must be the truth.
Sir Arthur Conan Doyle.

So without knowing anything about evolution creationists dismiss it as being false, how is that possible? I have never tasted a banana but I don't like them, does that make sense? I wonder if someone who knew as much as they do about evolution (nothing) told them it was false? who are these creationists? are they sheep or are they able to think for themselves?

Creationist biochemist Michael Behe tried to find fault with evolution and failed miserably, so what does the average
(or should I say under average) creationists think they can contribute? hot air is all they can contribute.

The fault lies in reading co,prehension and a reluctance on both sides to accept the synthesis that it suggests between Science and Theology:

 

[Zaius137]

To Naraoia…

“If only one ERV is allowed to undergo fixation at a time, which is bullcrap. Just how many polymorphisms exist in the human gene pool right now? You seem to have a persistent problem with parallel vs. sequential trials.”

How is that bullcrap??? You need to explain how more fixations can happen under neutral selection (non coding HERV’s). Suggestions like Synergistic epistasis need a selective agent.

I think "up to" 280 times is a lot less than you need to kick this particular p-value into non-significance...

Our last go around with probability was frustrating for me… I am not sure your suit is probability.

 

[Huram Abi]

The fault lies in reading co,prehension and a reluctance on both sides to accept the synthesis that it suggests between Science and Theology:

So, when I can't get a square peg in a round hole, it's because I'm not reading their descriptions on the packaging correctly?

Even though the description on their respective packaging says "square peg" and "round hole", that I can't force them together is my own fault?

In other words, if I just ignore what the packaging says (and the reality of the situation) and redefine "square" to mean "ovaloid" and redefine "round" to mean ovaloid (because it seems logical that an ovaloid peg should fit in an ovaloid hole) then these two pieces will suddenly and magically compliment each other, right?


This is the very reason experiments require "double-blind" testing: so that our biases don't define our expectations, our expectations don't define our idea of success, and our expectation of success does not cause us to discard relevant information that would show our failure.

 

[Zaius137]

“This is the very reason experiments require "double-blind" testing: so that our biases don't define our expectations, our expectations don't define our idea of success, and our expectation of success does not cause us to discard relevant information that would show our failure.”

By definition… (Double blind test)
A testing procedure, designed to eliminate biased results, in which the identity of those receiving a test treatment is concealed from both administrators and subjects until after the study is completed.


Double blind tests by definition do not fit the parameters for scientific experimentation. Science in its essence needs to define an experiment (create a hypothesis) based on an expectation. In the findings a conclusion can be drawn or data collected to that carefully defined domain of the experiment. A result can be fashioned.


To those in science:

• Ask a Question
• Do Background Research
• Construct a Hypothesis
• Test Your Hypothesis by Doing an Experiment
• Analyze Your Data and Draw a Conclusion
• Communicate Your Results

Here is the rub…

We all have biases and a comfy world view.

 

[Zaius137]

Sorry I did not get to these earlier…Nothing I can really say about your responses not lining up with what I said. It is just not consistent with the documentation I looked at. Try and read the following…as the famous line goes “The problem here... is a failure... to communicate”.

http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

That paper specifically looked at a class of ERVs that was not shared between humans and other apes. I assume you refer to this paragraph:

Please read the paragraph before this one carefully. They are talking about a comparison of chimps, gorillas, macaques and baboons. The human genome was used as a reference to map the sequences around the actual ERVs, it was not part of the comparison proper. Remember, PTERV1 insertions are absent from the human genome, so human PTERV1 insertions cannot be orthologous to anything. Because they don't exist.

Basically, it's their way of determining whether the insertions were orthologous in chimps, gorillas, macaques and baboons. Sequence a bit of the genomic neighbourhood of each insertion, map each to the human genome, and if two insertions in two different species map to the same region, they might be orthologous.

What the TalkOrigins article has to do with the above is a mystery. The section on ERVs looks like it hasn't even been updated since the human genome came out:

If only one ERV is allowed to undergo fixation at a time, which is bullcrap. Just how many polymorphisms exist in the human gene pool right now? You seem to have a persistent problem with parallel vs. sequential trials.

If you go back a few pages, I think Loudmouth posted evidence that retroviral insertions are pretty much random. They do have site preferences, but there are astronomical numbers of suitable sites in the genome.

I think "up to" 280 times is a lot less than you need to kick this particular p-value into non-significance...

 

[Huram Abi]

Double blind tests by definition do not fit the parameters for scientific experimentation.

Double blind tests are a part of testing a causal hypothesis but not forming one.

Blind tests are a very imprtant tool in many scientific experiments so that the results are not invalidated by the influence of expectation. It is a control to reduce error or self-deception.

 

[sfs]

To Naraoia…

“If only one ERV is allowed to undergo fixation at a time, which is bullcrap. Just how many polymorphisms exist in the human gene pool right now? You seem to have a persistent problem with parallel vs. sequential trials.”

How is that bullcrap???

It's bullcrap because it's completely wrong. Any number of neutral fixations can be occurring simultaneously. (Haldane's calculation also places no real limit on fixations due to selection, but that's irrelevant here.)

You need to explain how more fixations can happen under neutral selection (non coding HERV’s).

No, you need to offer some justification for thinking that neutral fixations are somehow limited, since that idea goes against everything known about genetics.

I think "up to" 280 times is a lot less than you need to kick this particular p-value into non-significance...

Our last go around with probability was frustrating for me… I am not sure your suit is probability.

If you use the 280x probability of insertion, your statistical argument will be hopeless. As the paper from which it was taken states, "Although we have sampled only a small fraction of the cell genome (-6000 of 2x 109 bases) the presence of integration targets in 12 of 12 regions sampled leads us to conclude that the majority of the cellular genome is available for integration and the total number of potential integration sites must be very large" [Genes Dev. 1994 8:1473-1487]. Yes, some sites within each region were more likely than others; if you look at their plots, it could be that as little as 10% of the genome is effectively available for ERV insertion. That would mean that each insertion has only 300,000,000 spots to choose from. The chance of getting a single insertion in the same place is 1 in 300,000,000, and the probability of getting multiple identical insertions is much, much smaller.

 

[sfs]

Sorry I did not get to these earlier…Nothing I can really say about your responses not lining up with what I said. It is just not consistent with the documentation I looked at. Try and read the following…as the famous line goes “The problem here... is a failure... to communicate”.

http://www.evolutionnews.org/2011/05/do_shared_ervs_support_common_046751.html

Ouch -- really a very weak response you've linked to. (And this from the top-shelf creationist organization, the Discovery Institute.) Start with the first argument:

In one relevant study, Barbulescu et al. (2001) report that,

We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome. Humans contain an intact preintegration site at this locus. [emphasis added]​

It seems that the most plausible explanation for this is an independent insert in the gorilla and chimpanzee lineages. Notice that the intact preintegration site at the pertinent locus in humans precludes the possibility of the HERV-K provirus having been inserted into the genome of the common ancestor of humans, chimpanzees and gorillas, and subsequently lost from the human genome by processes of genetic recombination. The inserts in the chimpanzee and gorilla lineages must be independent events.

The author assumes that the only reason that chimpanzees and gorillas, but not humans, would share an ERV insertion is that it inserted twice. He seems not to have heard of incomplete lineage sorting, or be aware that it is well known that chimps and gorillas are more closely related to each other than to humans in about one-sixth of their genome. (The same is true for humans and gorillas; humans and chimpanzees are only most closely related, genetically speaking, in two-thirds of their genome.) If an insertion site is shared among two of the species, one-sixth of the time it should be shared between chimps and gorillas, one-sixth between humans and gorillas and two-thirds of the time between humans and chimps. Zero points for this one.

Then comes the 280x insertion probability, which I dealt with in another post. Then comes this bit:

In addition,Yohn et al. (2005) report that,

Horizontal transmissions between species have been proposed, but little evidence exists for such events in the human/great ape lineage of evolution. Based on analysis of finished BAC chimpanzee genome sequence, we characterize a retroviral element (Pan troglodytes endogenous retrovirus 1 [PTERV1]) that has become integrated in the germline of African great ape and Old World monkey species but is absent from humans and Asian ape genomes.​

Yohn et al are talking about a retrovirus that infected both African great apes and Old World monkeys, but not humans. It is not talking about identical insertion points in great apes and monkeys, which really would be a strong piece of evidence against ERVs as markers of common descent. In fact, the paper sets a lower bound of 95.8% on the fraction of shared insertion sites. Did the the author not read the paper in question (or even the entire abstract, since the 95.8% number is there)? Is he simply clueless about the subject he's writing about?

I guess this is the best creationists can do.

 

[Zaius137]

Where you bin sfs? Good to reason with you again.

"It's bullcrap because it's completely wrong. Any number of neutral fixations can be occurring simultaneously. (Haldane's calculation also places no real limit on fixations due to selection, but that's irrelevant here.)”

It does not matter where or how often the insertions take place. To be fixed in a population Haldane is very clear about the 300 generations per insertion. You missed my point about neutral selection all together. In this case there can be no rescue from Haldane by simply waiving the hands and causing mass fitness selections in the population (because it is neutral). The calculation as I currently understand it puts the timescale at least 10 times what the evolutionist paradigm claims and out of reach of a common ancestor explanation. All evolutionists can do is attack Haldane’s conclusion but it has even found support amongst a few of them.


“Yohn et al are talking about a retrovirus that infected both African great apes and Old World monkeys, but not humans. It is not talking about identical insertion points in great apes and monkeys, which really would be a strong piece of evidence against ERVs as markers of common descent. In fact, the paper sets a lower bound of 95.8% on the fraction of shared insertion sites. Did the the author not read the paper in question (or even the entire abstract, since the 95.8% number is there)? Is he simply clueless about the subject he's writing about?”

Yes the point is that the ERV (HERV-k) is in the great apes and the chimps but not in humans. If the human and chimp were common ancestors the insertion (since it is in the apes today) should be in humans… it is not. Genetic recombination is not a likely explanation for this anomaly because Humans contain an intact preintegration site at this locus. As for the rest of your review it is clear that you disagree with author and my citations. But I see no substantial argument here, just more hand waiving.

 

[cupid dave]

It is clear that Genesis and Science are rather supportive to one another when look at the sum of what is written.

There was a beginning, with a Big Bang.

The Clock of the Eras tick off the seven "days."

There are 22 names in the genesis genealogy and there are 22 species in the Ascent of Modern man as far was we now know.

Plant life did appear before animal life.

The was a Pangea surrounded by one ocean of water.

There was a Cosmic Dark Age before god said "let there be light.'

etc

 

[Huram Abi]

It is clear that Genesis and Science are rather supportive to one another when look at the sum of what is written.

There was a beginning, with a Big Bang.

The Clock of the Eras tick off the seven "days."

There are 22 names in the genesis genealogy and there are 22 species in the Ascent of Modern man as far was we now know.

Plant life did appear before animal life.

The was a Pangea surrounded by one ocean of water.

There was a Cosmic Dark Age before god said "let there be light.'

etc

Red= not supported by science

Blue= not supported by the bible

Green= not supported by science or the bible

None of these are evidence for your claim.

 

[sfs]

"It's bullcrap because it's completely wrong. Any number of neutral fixations can be occurring simultaneously. (Haldane's calculation also places no real limit on fixations due to selection, but that's irrelevant here.)”

It does not matter where or how often the insertions take place. To be fixed in a population Haldane is very clear about the 300 generations per insertion.

Wrong. Haldane said nothing about neutral fixation at all.

You missed my point about neutral selection all together. In this case there can be no rescue from Haldane by simply waiving the hands and causing mass fitness selections in the population (because it is neutral). The calculation as I currently understand it puts the timescale at least 10 times what the evolutionist paradigm claims and out of reach of a common ancestor explanation. All evolutionists can do is attack Haldane’s conclusion but it has even found support amongst a few of them.

Haldane is completely irrelevant here.

“Yohn et al are talking about a retrovirus that infected both African great apes and Old World monkeys, but not humans. It is not talking about identical insertion points in great apes and monkeys, which really would be a strong piece of evidence against ERVs as markers of common descent. In fact, the paper sets a lower bound of 95.8% on the fraction of shared insertion sites. Did the the author not read the paper in question (or even the entire abstract, since the 95.8% number is there)? Is he simply clueless about the subject he's writing about?”

Yes the point is that the ERV (HERV-k) is in the great apes and the chimps but not in humans.

Yes, they were infected with the same virus. So?

If the human and chimp were common ancestors the insertion (since it is in the apes today) should be in humans… it is not.

Also wrong. They should share the insertion point only if their common ancestor was infected with the virus and an insertion occurred in that population. Instead, the descendents were infected and therefore should not share insertion points.

Genetic recombination is not a likely explanation for this anomaly because Humans contain an intact preintegration site at this locus.

There is no anomaly, only a failure to understand what the paper was about.

As for the rest of your review it is clear that you disagree with author and my citations. But I see no substantial argument here, just more hand waiving.

You never see substantial arguments because you don't understand the issues.