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Is the Human Brain a Null Hypothesis for Darwinian Evolution?

Can the Evolution of the Human Brain be a Basis for a Null Hypothesis of Darwinism?


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Loudmouth

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Well for starters:

Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common. (Estimate of the Mutation Rate per Nucleotide in Humans. Genetics, Vol. 156, 297-304, September 2000)​

That's at 1.33%, what happens when the divergence jumps to 4%:

It doesn't jump to 4%. The substitution rate is 1.33% in coding regions, which is what they are discussing.

Since the rest of your argument is based on this false assumption, we can ignore the rest of it.

Invariably you point to some obscure semantic correction only to bury the evidence in this kind of pedantic rationalization.

You invariably try to justify your continued rejection of the facts with these lines of argumentation.

Except you are assuming the ERVs are the result of highly deleterious germline invasions resulting in 8% of the human genome overall.

If they were highly deleterious, how can we survive with 8% of our genome being made up of ERV's?


That flies in the face of the fact that ERVs are so different between species that are assumed to have common ancestry.

More than 99.9% of the ERV's found in humans are found at the same location in the chimp genome. Finding less than 300 ERV's that have occurred since the divergence of the chimp and human lineage does nothing to negate the fact that we share over 200,000 ERV's at the same location in each of our genomes.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). They can be found in African great apes but not in humans. What is more the ERV virus is nearly extinct in the human genome with only a couple that actually work. The only thing that ERVs are proof of is the lengths evolutionists will go to to conflate and confuse the evidence.

There are over 200,000 ERVs in the human and chimp genome. Still ignoring that fact?

For almost half a century it was believed that Chimpanzee and Human DNA was virtually identical. This is now known to be false. The Comparison of Human Chromosome 21 and Chimpanzee Chromosome 22 revealed that 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level. These included gross structural changes affecting gene products far more common than previously estimated (20.3% of the PTR22 proteins) (Nature, 27 May 2004).

98% identical means that they are 2% not-identical. Most people consider that to be virtually identical. Pointing to the 2% difference won't make the 98% identical sequence go away.

Why, so you can ask the question in circles? That's what we are talking about, the divergence is too great to be accounted for by mutations.

That claim has already been refuted.
 
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mark kennedy

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It doesn't jump to 4%. The substitution rate is 1.33% in coding regions, which is what they are discussing.

No, we are discussing divergence and that particular statistic is from psuedogenes which are not within the functional and coding genes.

Since the rest of your argument is based on this false assumption, we can ignore the rest of it.

Everything in Darwinian logic is false assumption so we can dismiss that as well. Which leaves us with what exactly?

You invariably try to justify your continued rejection of the facts with these lines of argumentation.

As always you have abandoned the facts in favor of pedantic one liners. Way to stay consistent.

If they were highly deleterious, how can we survive with 8% of our genome being made up of ERV's?

A question you should have asked yourself before you assumed they were the result of these highly deleterious and suppositional germline invasions. We couldn't, that's the point.


More than 99.9% of the ERV's found in humans are found at the same location in the chimp genome. Finding less than 300 ERV's that have occurred since the divergence of the chimp and human lineage does nothing to negate the fact that we share over 200,000 ERV's at the same location in each of our genomes.

Which you should be backing with real world statistics and data, something I have never seen from you.

There are over 200,000 ERVs in the human and chimp genome. Still ignoring that fact?


With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact?


98% identical means that they are 2% not-identical. Most people consider that to be virtually identical. Pointing to the 2% difference won't make the 98% identical sequence go away.

83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level. These included gross structural changes affecting gene products far more common than previously estimated (20.3% of the PTR22 proteins) (Nature, 27 May 2004).

When you actually look at what the divergence is, including the protein coding genes, the difference never goes away.

That claim has already been refuted.

The deleterious effect of the requisite mutations has never been addressed, much less refuted.

Don't you get dizzy arguing these pedantic, fallacious arguments in circles? You should. You have neglected the actual question of the thread. let me break it down for you. If the similarities are proof of common ancestry then are the differences evidence to the contrary?

Your dodging the question, as usual. There is a reason for that, you can't honestly answer it.

Have a nice day :)
Mark
 
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mark kennedy

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It sure seems to me that your attack on scientists are inappropriate ad hominem attacks. Funny, how they keep ignoring all these things you point out as significant. Maybe you should instruct them? Also, you failed to answer my question about gills. Why should anything have a structure ever resembling gills if it is a process totally independent of the development of gills? Another member provided the appropriate answer.

I don't attack scientists, I attack Darwinism. Those are not gills and no one has made a substantive argument to the contrary because they can't. You are begging the question of proof on your hands and knees and your arguments are shrinking down do fallacious ad hominem attacks which indicates you have nothing else.

Inevitable.

Have a nice day :)
Mark
 
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Loudmouth

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Everything in Darwinian logic is false assumption so we can dismiss that as well. Which leaves us with what exactly?

What are these false assumptions?

A question you should have asked yourself before you assumed they were the result of these highly deleterious and suppositional germline invasions. We couldn't, that's the point.

If they are highly deleterious, how are humans able to survive with 8% of our genome being made up of inserted retroviruses? The facts disprove your claims. We are able to tolerate them just fine.

Which you should be backing with real world statistics and data, something I have never seen from you.

I already have on multiple instances, including conversations with you.

Human genome paper, Table 11. This table shows over 200,000 in the human genome.

409860at-011.gif

http://www.nature.com/nature/journal/v409/n6822/fig_tab/409860a0_T11.html

Table 2 from the chimp genome paper. It shows less than 300 chimp specific ERVs and less than 100 human specific ERVs.

nature04072-t2.jpg

http://www.nature.com/nature/journal/v437/n7055/fig_tab/nature04072_T2.html

This means that out of 200,000 ERVs found in the human genome, all but 100 are found at the same location in the chimp genome. Out of the 200,000+ ERVs in the chimp genome, all but 300 are found at the same location in the human genome.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact?

I have fully incorporated the fact, as shown by the table above. I show that chimps have about 300 species specific insertions, most of them being PtERV insertions.

Did you also forget that the paper you are referencing only looked at 425 ERVs in total?

"Using the procedure described above, we identified a total of 425 full-length chimpanzee endogenous retroviruses. This is certainly an underestimate of the number of endogenous retroviruses in the chimpanzee genome because we consciously excluded any sequences that could not be unambiguously identified as an endogenous retrovirus."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779541/

Are you still ignoring this fact?


83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level. These included gross structural changes affecting gene products far more common than previously estimated (20.3% of the PTR22 proteins) (Nature, 27 May 2004).

When you actually look at what the divergence is, including the protein coding genes, the difference never goes away.

Why would we have to ignore the differences? The differences are what evolution is all about. Those differences are the end product of evolution, after all.

The deleterious effect of the requisite mutations has never been addressed, much less refuted.

You would first need to show that they are deleterious.

Don't you get dizzy arguing these pedantic, fallacious arguments in circles? You should. You have neglected the actual question of the thread. let me break it down for you. If the similarities are proof of common ancestry then are the differences evidence to the contrary?

Have you already forgotten our previous conversation on this subject?

We aren't making a similarity argument.

Let me repeat.

We aren't making a similarity argument.

We are arguing that evolution is supported by the observed pattern of both similarities AND DIFFERENCES. That pattern is a nested hierarchy. We are making a phylogenetic argument, not a similarity argument. It is the match between the tree based on morphology and the tree based on DNA sequences that evidence evolution, and those trees are based on both similarities and differences.
 
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Loudmouth

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I don't attack scientists, I attack Darwinism. Those are not gills and no one has made a substantive argument to the contrary because they can't. You are begging the question of proof on your hands and knees and your arguments are shrinking down do fallacious ad hominem attacks which indicates you have nothing else.

Inevitable.

Have a nice day :)
Mark

They do develop into gills in fish, and you have not made a substantive argument otherwise.
 
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Loudmouth

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I find it hard to believe that evolutionary apologists so often ignore the work of scientists who directly observe and describe the deleterious effects of mutations.

Finding a deleterious mutation does not mean that all mutations are deleterious. Simple logic, yet you can't figure it out.

Are the 40 million mutations that separate the human and chimp genome deleterious to humans? Yes or no?

I'm not contradicting anything in the scientific literature, I invariably quote, cite and often link to it as definitive evidence. To date, not one evolutionist has made a substantive argument explaining the indels. Instead they just ignore them:

On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions. (Initial Sequence of the Chimpanzee genome, Nature)
That's when I know you have nothing else, when all your pedantic arguments finally boil down into ad hominem retorts. I don't claim to know more, just continue to point out the obvious deleterious effects of such large scale mutations. It's not a formula for adaptive evolution, it's a formula for extinction.

Have a nice day :)
Mark

Pointing to divergence between genomes is a problem for a theory that explains how nature produces divergence between genomes? Really?

What next? Will you point to modern river eroding a valley as evidence against the theory that rivers erode valleys? Will you point to bacteria causing disease as a disproof of the germ theory of disease?

Do you even understand what the theory of evolution proposes?

What is it about indels that you think needs explaining?
 
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mark kennedy

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What are these false assumptions?

They start with this one:

The doctrine that species, including man, are descended from other species. He first did the eminent service of arousing attention to the probability of all change in the organic, as well as in the inorganic world, being the result of law, and not of miraculous interposition. (Darwin, On the Origin of Species)​

Then they grow to include viral germline invasions that would be a formula for extinction.

If they are highly deleterious, how are humans able to survive with 8% of our genome being made up of inserted retroviruses? The facts disprove your claims. We are able to tolerate them just fine.

We didn't survive them, those are broken reading frames, nothing more. That's another false assumption of a cause that cannot be proven or even explained.

I already have on multiple instances, including conversations with you.

Human genome paper, Table 11. This table shows over 200,000 in the human genome.

409860at-011.gif

http://www.nature.com/nature/journal/v409/n6822/fig_tab/409860a0_T11.html

Table 2 from the chimp genome paper. It shows less than 300 chimp specific ERVs and less than 100 human specific ERVs.

nature04072-t2.jpg

http://www.nature.com/nature/journal/v437/n7055/fig_tab/nature04072_T2.html

Against this background, it was surprising to find that the chimpanzee genome has two active retroviral elements (PtERV1 and PtERV2) that are unlike any older elements in either genome; these must have been introduced by infection of the chimpanzee germ line. The smaller family (PtERV2) has only a few dozen copies, which nonetheless represent multiple (~5–8) invasions, because the sequence differences among reconstructed subfamilies are too great (~8%) to have arisen by mutation since divergence from human. (Chimpanzee Genome, Nature 2005)
That's not the only surprise.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact!​

You left out greater then a million base pairs.

This means that out of 200,000 ERVs found in the human genome, all but 100 are found at the same location in the chimp genome. Out of the 200,000+ ERVs in the chimp genome, all but 300 are found at the same location in the human genome.

That's twice in one post you did that. First you beg the question of proof with regards to viral germline invasions becoming permanently fixed. Then you pretend that the ones in the Chimpanzee genome are exactly the same as the ones in humans which is clearly contradicted by the facts:

PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species (Chimpanzee Genone)
I have fully incorporated the fact, as shown by the table above. I show that chimps have about 300 species specific insertions, most of them being PtERV insertions.

You quoted and posted the table, just left out an actual argument.

Did you also forget that the paper you are referencing only looked at 425 ERVs in total?

"Using the procedure described above, we identified a total of 425 full-length chimpanzee endogenous retroviruses. This is certainly an underestimate of the number of endogenous retroviruses in the chimpanzee genome because we consciously excluded any sequences that could not be unambiguously identified as an endogenous retrovirus."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1779541/

No

We identified a total of 425 full-length chimpanzee endogenous retroviruses. This is certainly an underestimate of the number of endogenous retroviruses in the chimpanzee genome because we consciously excluded any sequences that could not be unambiguously identified as an endogenous retrovirus. (Genome Biol. 2006)​

Are you still ignoring this fact?

Are you completely oblivious to the context of the statement?

Why would we have to ignore the differences? The differences are what evolution is all about. Those differences are the end product of evolution, after all.

An assumed evolutionary process, as applied to a natural history that is little more then a myth.

You would first need to show that they are deleterious.

You think I need to prove that germline invasions are deleterious? Not really interested in chasing that one around the mulberry bush.

hbfig4.gif


The diversity of the earliest stages of development, here illustrated strictly within the vertebrates, provides one of the strongest challenges to the neo-Darwinian conception of homology and macroevolution. Given the hierarchical, step-wise logic or "architecture" of animal development, early stages such as cleavage and gastrulation lay the groundwork for all that follows. Body plan structures in the adult, for example, trace their cellular lineage to these early stages. Thus, if macroevolution is going to occur, it must begin in early development. Yet it is precisely here, in early development, that organisms are least tolerant of mutations. Furthermore, the adult homologies shared by these vertebrates commence at remarkably different points (e.g., cleavage patterns). How then did these different starting points evolve from a common ancestor? (Homology: A Concept in Crisis)​

That's just for starters, when mutations have an effect, and ERVs would definitely would have an effect on germline cells, they are almost always deleterious. In the case of germline cells they would most likely be fatal. Darwinism doesn't have to worry about that because an assumed ancient and prehistoric history is never questioned.

We are arguing that evolution is supported by the observed pattern of both similarities AND DIFFERENCES. That pattern is a nested hierarchy. We are making a phylogenetic argument, not a similarity argument. It is the match between the tree based on morphology and the tree based on DNA sequences that evidence evolution, and those trees are based on both similarities and differences.

We huh? In case you missed it the crowd isn't turning into a mob as they did in the past. At any rate you are obviously trying to mimic an homology argument, that much is obvious. What you seem unwilling or unable to come to terms with is the enormous diversity and an obvious inverse logic. If the similarities are evidence for common ancestry are the differences an argument for independent lineage? The inverse logic is intuitively obvious. What's more you pretend that they are identical in humans and chimpanzees and nothing could be further from the truth.

They do develop into gills in fish, and you have not made a substantive argument otherwise.

No they don't and no you haven't.

Finding a deleterious mutation does not mean that all mutations are deleterious. Simple logic, yet you can't figure it out.

Are the 40 million mutations that separate the human and chimp genome deleterious to humans? Yes or no?

They are differences, 35 million base pair differences and 5 million gaps totaling about 90 million base pairs of divergence. They are only assumed to be the result of mutations, just like the ERVs, just like the three fold expansion of the human brain from that of apes.

Pointing to divergence between genomes is a problem for a theory that explains how nature produces divergence between genomes? Really?

We are talking about comparative genomics, the explanation for how those differences came about begs the question of proof on it's hands and knees.

What next? Will you point to modern river eroding a valley as evidence against the theory that rivers erode valleys? Will you point to bacteria causing disease as a disproof of the germ theory of disease?

Pull up dude, you going into a pedantic, sardonic downward spiral.

Do you even understand what the theory of evolution proposes?

Do you even know what the word means? How about the words genomic comparison, do you get what that means?

What is it about indels that you think needs explaining?

They are not indels, the are gaps in the sequences that exist in one sequence but not in the other. It never ceases to amaze me how such devout evolutionists fail to understand the most basic and obvious facts. I lost interest in the subject matter after it got to be fish in a barrel. What really interests me are the evolutionists who seem incapable of basic insights and cursory reading. Curious, very curious indeed.


Have a nice day :)
Mark
 
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Loudmouth

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They start with this one:

The doctrine that species, including man, are descended from other species. He first did the eminent service of arousing attention to the probability of all change in the organic, as well as in the inorganic world, being the result of law, and not of miraculous interposition. (Darwin, On the Origin of Species)​

Then they grow to include viral germline invasions that would be a formula for extinction.

Common ancestry between humans and other species is not assumed. It is a well evidenced conclusion.

We didn't survive them, those are broken reading frames, nothing more.

I don't see why they can't be ERVs and have frame shift mutations. Can you explain this?

1. They have all of the features of a retrovirus: LTRs, gag, env, and pol genes.

2. Consensus sequences derived from HERV-K insertions produce viable retroviruses.

These two facts alone are smoking-gun evidence that ERVs are the product of retroviral insertions.

That's another false assumption of a cause that cannot be proven or even explained.

It is as proven as a fingerprint being the product of a fingertip.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact!

I already addressed it. It is the most abundant family out of the 425 ERVs they looked at. There are over 200,000 total ERVs in the chimp genome.

Still ignoring these facts?


First you beg the question of proof with regards to viral germline invasions becoming permanently fixed.

I supplied the evidence. No assumptions are being made.

Then you pretend that the ones in the Chimpanzee genome are exactly the same as the ones in humans which is clearly contradicted by the facts:

PtERV1-like elements are present in the rhesus monkey, olive baboon and African great apes but not in human, orang-utan or gibbon, suggesting separate germline invasions in these species (Chimpanzee Genone)

I never said that they are exactly alike. Here is what I said in post #81:

More than 99.9% of the ERV's found in humans are found at the same location in the chimp genome. Finding less than 300 ERV's that have occurred since the divergence of the chimp and human lineage does nothing to negate the fact that we share over 200,000 ERV's at the same location in each of our genomes.

How many times do I need to repeat this?

You quoted and posted the table, just left out an actual argument.

And here is the argument:

"Given the size of vertebrate genomes (>1 × 10^9 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14)."
http://www.pnas.org/content/96/18/10254.full

There are over 200,000 human ERVs that are found at the same exact spot in the chimp genome. That is proof beyond any reasonable doubt for common ancestry.



No

We identified a total of 425 full-length chimpanzee endogenous retroviruses. This is certainly an underestimate of the number of endogenous retroviruses in the chimpanzee genome because we consciously excluded any sequences that could not be unambiguously identified as an endogenous retrovirus. (Genome Biol. 2006)​



Are you completely oblivious to the context of the statement?

The comparisons of chimp ERVs in that paper are dealing with the 425 they identified. They did not survey all 200,000 ERVs in the chimp genome. Are you completely oblivious to the context of that statement?

An assumed evolutionary process, as applied to a natural history that is little more then a myth.

We have the evidence. It isn't a myth.

You think I need to prove that germline invasions are deleterious?

If you want to claim that every single insertion of a retrovirus is deleterious, then you have to prove it.
The diversity of the earliest stages of development, here illustrated strictly within the vertebrates, provides one of the strongest challenges to the neo-Darwinian conception of homology and macroevolution. Given the hierarchical, step-wise logic or "architecture" of animal development, early stages such as cleavage and gastrulation lay the groundwork for all that follows. Body plan structures in the adult, for example, trace their cellular lineage to these early stages. Thus, if macroevolution is going to occur, it must begin in early development. Yet it is precisely here, in early development, that organisms are least tolerant of mutations. Furthermore, the adult homologies shared by these vertebrates commence at remarkably different points (e.g., cleavage patterns). How then did these different starting points evolve from a common ancestor? (Homology: A Concept in Crisis)

That's just for starters, when mutations have an effect, and ERVs would definitely would have an effect on germline cells, they are almost always deleterious. In the case of germline cells they would most likely be fatal. Darwinism doesn't have to worry about that because an assumed ancient and prehistoric history is never questioned.

You need to demonstrate that every retrovirus insertion would have an affect. Just asserting it won't do.

We huh? In case you missed it the crowd isn't turning into a mob as they did in the past. At any rate you are obviously trying to mimic an homology argument, that much is obvious.

I am making a phylogenetic argument, for the thousandth time. It is the pattern of both similarities and differences that evidence evolution.

What you seem unwilling or unable to come to terms with is the enormous diversity and an obvious inverse logic.

The inverse logic would be multiple and obvious violations of a nested hierarchy. That is what would disprove evolution.

If the similarities are evidence for common ancestry are the differences an argument for independent lineage?

The phylogenies are evidence of common ancestry, not the similarities.

No they don't and no you haven't.

Then what structures in fish embryos develop into gills?

They are differences, 35 million base pair differences and 5 million gaps totaling about 90 million base pairs of divergence. They are only assumed to be the result of mutations, just like the ERVs, just like the three fold expansion of the human brain from that of apes.

They are demonstrated to be mutations as shown by sequence conservation between species and the observed nested hierarchies. Yet more evidence that you run away from.

We are talking about comparative genomics, the explanation for how those differences came about begs the question of proof on it's hands and knees.

If those differences are the result of mutations and natural selection, then we would expect to see different divergence rates between introns and exons. Since the exons are used to produce the resulting amino acid sequence, they are much more susceptible to deleterious mutations compared to the introns that are clipped out of RNA to produce mature mRNA. Therefore, there should be selection against some mutations in exons compared to introns if mutations are both random and selection is acting on species over time. This will result in introns accumulating more mutations over time than exons. Is this what we see? Yep, sure is.


upload_2016-6-16_14-17-51.png


upload_2016-6-16_14-18-52.png

https://tulsa.younglife.org/Documents/Francis Collins Article on Faith_Science.pdf

When you see both sequence conservation and phylogenies, this is proof beyond any reasonable doubt that mutations and selection are responsible for the differences between species.

Do you even know what the word means? How about the words genomic comparison, do you get what that means?

Evolution means CHANGE over time, right? How is pointing to change a problem for the very theory that expects to see change?


They are not indels, the are gaps in the sequences that exist in one sequence but not in the other. It never ceases to amaze me how such devout evolutionists fail to understand the most basic and obvious facts. I lost interest in the subject matter after it got to be fish in a barrel. What really interests me are the evolutionists who seem incapable of basic insights and cursory reading. Curious, very curious indeed.

How are these gaps in sequence a problem for the theory of evolution?

You do know that we have directly observed indel mutations, right?
 
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mark kennedy

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I fail to see how any of this would point to a God of any description.

Because you refuse to accept the alternative to naturalistic assumptions.

I don't know how this all works therefore a God did it.

I fail to see how God didn't do it is an explanation.

I don't know where everything came from therefore a God did it.

It's not based on what you don't know but what you do know. I do know where everything came from therefore I'm not limited to exclusively naturalistic explanations.

Have a nice day :)
Mark
 
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mark kennedy

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Common ancestry between humans and other species is not assumed. It is a well evidenced conclusion.

The a priori assumption of universal common descent was never a conclusion. Otherwise the alternative would be considered and it never is.

I don't see why they can't be ERVs and have frame shift mutations. Can you explain this?

Yes, because they are protein coding gene reading frames that happen to be broken.

1. They have all of the features of a retrovirus: LTRs, gag, env, and pol genes.

I know how they are characterized, so what?

2. Consensus sequences derived from HERV-K insertions produce viable retroviruses.

The HERV-K still works, again so what?

These two facts alone are smoking-gun evidence that ERVs are the product of retroviral insertions.

You are confusing cause with effect. All you have done is to make some pedantic generalizations about the characteristics of ERVs, that's not the same thing as demonstrating how they became permanently fixed in the human genome.

It is as proven as a fingerprint being the product of a fingertip.

Except it doesn't happen in the human genome now.

I already addressed it. It is the most abundant family out of the 425 ERVs they looked at. There are over 200,000 total ERVs in the chimp genome.

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact!

Still ignoring these facts?

The facts are not in question. The cause is still being begged on you hands and knees.

I supplied the evidence. No assumptions are being made.

Your argument is shrinking to pedantic one liners. Pull up dude!


I never said that they are exactly alike. Here is what I said in post #81:

More than 99.9% of the ERV's found in humans are found at the same location in the chimp genome. Finding less than 300 ERV's that have occurred since the divergence of the chimp and human lineage does nothing to negate the fact that we share over 200,000 ERV's at the same location in each of our genomes.

How many times do I need to repeat this?

No their not, that's not a quote, that's a gross overestimation.



And here is the argument:

"Given the size of vertebrate genomes (>1 × 10^9 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24). Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place (14)."
http://www.pnas.org/content/96/18/10254.full

An assumption based on this referenced statement which is nothing more then three insertions:

Comparison of the nucleotide sequences of the three elements leads to the hypothesis that foreign DNA introduced into the genome can initially accumulate mutations more rapidly than the genomic sequences surrounding it. (Three independent insertions of retrovirus-like sequences in the haptoglobin gene cluster of primates. Genomics 1990)​

A paper published, I might add, ten years before the Initial Sequence of the Human Genome.

There are over 200,000 human ERVs that are found at the same exact spot in the chimp genome. That is proof beyond any reasonable doubt for common ancestry.

No their are not. There are ERVs described in the Human Genome paper and else where but no one has argued that they are all at the same location in both genomes. You are simply making that up.



The comparisons of chimp ERVs in that paper are dealing with the 425 they identified. They did not survey all 200,000 ERVs in the chimp genome. Are you completely oblivious to the context of that statement?

Because it's a fabrication.

We have the evidence. It isn't a myth.

Nonsense.

You need to demonstrate that every retrovirus insertion would have an affect. Just asserting it won't do.

Where and when are they inserted because if you are talking the cleavage stage you are grasping at straws.

I am making a phylogenetic argument, for the thousandth time. It is the pattern of both similarities and differences that evidence evolution.

You are making the same failed argument you have made a thousand times, in circles.



The inverse logic would be multiple and obvious violations of a nested hierarchy. That is what would disprove evolution.

Evolution is a phenomenon not a theory. Nothing disproves it. You are equivocating evolution with Darwinian naturalistic assumptions. Darwinism has a null hypothesis, it's the human brain.



The phylogenies are evidence of common ancestry, not the similarities.

The divergence is proof of independent lineage, the inverse logic is intuitively obvious.


Then what structures in fish embryos develop into gills?

It's not the ears. They don't have any.

They are demonstrated to be mutations as shown by sequence conservation between species and the observed nested hierarchies. Yet more evidence that you run away from.

Drifting so far from actual specifics must be a lonely feeling.

When you see both sequence conservation and phylogenies, this is proof beyond any reasonable doubt that mutations and selection are responsible for the differences between species.

No not really and it's kind of boring to watch you play with the word salad.

Evolution means CHANGE over time, right? How is pointing to change a problem for the very theory that expects to see change?

The change of alleles in populations over time. It's not a theory, it's a phenomenon.

How are these gaps in sequence a problem for the theory of evolution?

Because you have to explain how they got there, not just assume they are the result of mutations.

You do know that we have directly observed indel mutations, right?

Directly observed genomic comparisons or actual mutations?

You sure ran out of gas quick. I hope to be back to shoot fish in a barrel later. This is fun, it's nice to finally have these pointless rationalizations isolated.

Have a nice day :)
Mark
 
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Jimmy D

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Because you refuse to accept the alternative to naturalistic assumptions.



I fail to see how God didn't do it is an explanation.



It's not based on what you don't know but what you do know. I do know where everything came from therefore I'm not limited to exclusively naturalistic explanations.

Have a nice day :)
Mark

You seem like an intelligent fellow Mark, I'm sure you're already aware that you a presenting a false dichotomy. Just because one naturalistic explanation may not be correct doesn't mean that another won't be. It also seems fairly arrogant to suggest that you know where everything comes from, rather than attempting to pick holes in the TOE wouldn't it be more productive share this wisdom with us?
 
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Loudmouth

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The a priori assumption of universal common descent was never a conclusion. Otherwise the alternative would be considered and it never is.

The alternative was considered. It is called the null hypothesis.

If genome comparisons did not fall into the same nested hierarchy as that formed by morphology, then we would have concluded that common ancestry was not supported.

The alternative is built into every genome comparison between multiple species. It is a part of the scientific method.

Yes, because they are protein coding gene reading frames that happen to be broken.

So why can't a stretch of DNA be from a retrovirus and also have indel mutations? Please explain.

I know how they are characterized, so what?

We can directly observe retroviruses producing ERVs in the lab. The ERVs in primate genomes have all of the retroviral genes and features. Why shouldn't we conclude that they came from retroviral insertion?

The HERV-K still works, again so what?

So you are ignoring the evidence that ERVs came from retroviral insertion.

You are confusing cause with effect. All you have done is to make some pedantic generalizations about the characteristics of ERVs, that's not the same thing as demonstrating how they became permanently fixed in the human genome.

We can observe in the lab how they become permanently fixed in the human genome. They insert into the genome. They are then copied as part of the normal DNA replication of the host genome. Are you really not aware of this?

Except it doesn't happen in the human genome now.

We can directly observe retroviruses inserting into human genomes. There are several studies where they introduce retroviruses to human cells, and then map the resulting ERVs in the human cells.

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020234

With more than 100 members, CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. (Genome Biol. 2006). Still ignoring that fact!

There are over 200,000 ERVs in the chimp genome. Still ignoring this fact?

Are you also still ignoring the fact that the study you are referencing only looked at 425 ERVs?


The facts are not in question.

You are questioning the facts. I have shown you the fact that the human genome contains over 200,000 ERVs. I have shown you the fact that less than 100 are not found at the same exact spot in the chimp genome. You refuse to accept those facts.

I have shown you the table from the human genome paper listing 200,000 ERVs in the human genome paper.

I have shown you the table from the chimp genome paper where they compared the human and chimp genomes, and they found less than 100 human ERVs that were not found at the same location in the chimp genome. They found less that 300 out of 200,000 ERVs in the chimp genome that were specific to chimps. The rest were found at the same location in the human genome.

THOSE ARE THE FACTS. I have supported them with scientific references, and yet you refuse to accept these facts because you don't like them. They aren't fabrications. They are facts.

An assumption based on this referenced statement which is nothing more then three insertions:

Comparison of the nucleotide sequences of the three elements leads to the hypothesis that foreign DNA introduced into the genome can initially accumulate mutations more rapidly than the genomic sequences surrounding it. (Three independent insertions of retrovirus-like sequences in the haptoglobin gene cluster of primates. Genomics 1990)​

The placement of the ERVs in the genome is not based on that assumption.

A paper published, I might add, ten years before the Initial Sequence of the Human Genome.

You don't need to sequence the entire genome in order to determine if the ERVs are found at the same locus. You only need to sequence the genome upstream and downstream of the ERV.

No their are not. There are ERVs described in the Human Genome paper and else where but no one has argued that they are all at the same location in both genomes. You are simply making that up.

It is exactly what the authors of the chimp genome paper are arguing. By listing the species specific ERVs, they are arguing that the rest of the ERVs are not species specific. Do you know how they determine if an ERV is species specific or not? They look to see if the ERV is in the same location in both species. That's how they do it.

Because it's a fabrication.

Denial of facts.

Nonsense.

Denial of facts.

Where and when are they inserted because if you are talking the cleavage stage you are grasping at straws.

Please show that every single retroviral insertion will be harmful to the host. That is your claim, and you need to support it.

You are making the same failed argument you have made a thousand times, in circles.

You have yet to refute the argument, so I will repeat it until you do.
Evolution is a phenomenon not a theory. Nothing disproves it. You are equivocating evolution with Darwinian naturalistic assumptions. Darwinism has a null hypothesis, it's the human brain.

A lack of a nested hierarchy would disprove it, as I have said over and over and over. It is the nested hierarchy that evidences the theory of evolution, and a nested hierarchy incorporates both similarities and differences.

The divergence is proof of independent lineage, the inverse logic is intuitively obvious.

The inverse logic would be that conservation of sequence is proof of shared lineage. Since we find conserved sequence, then that is proof of common ancestry.

What we have is a mixture of shared DNA from common ancestry and independently evolved sequence. That is EXACTLY WHAT EVOLUTION SHOULD PRODUCE.

Do you really not know how evolution works?

It's not the ears. They don't have any.

Then what is it? What features in the fish embryo develop into gills?

The change of alleles in populations over time. It's not a theory, it's a phenomenon.

Do a google search for "theory of evolution".

Because you have to explain how they got there, not just assume they are the result of mutations.

Already explained that.


Directly observed genomic comparisons or actual mutations?

Both. We can sequence a child's genome and the genome of that child's parents. Guess what we find? Mutations.
 
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mark kennedy

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You seem like an intelligent fellow Mark, I'm sure you're already aware that you a presenting a false dichotomy. Just because one naturalistic explanation may not be correct doesn't mean that another won't be. It also seems fairly arrogant to suggest that you know where everything comes from, rather than attempting to pick holes in the TOE wouldn't it be more productive share this wisdom with us?

There is no dichotomy, the problem is that the only alternative to naturalistic evolution is God, as cause of anything, is rejected a priori (without prior). I don't have a problem with evolution, God doesn't even get credit as designer. Obviously, an a priori assumption of universal common descent going all the way back to, and including, the Big Bang. That's not science, that's supposition.

Have a nice day :)
Mark
 
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mark kennedy

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The alternative was considered. It is called the null hypothesis.

Oh but you don't do null hypothesis or we would be talking about the human brain.

If genome comparisons did not fall into the same nested hierarchy as that formed by morphology, then we would have concluded that common ancestry was not supported.

Taxonomy is organized based on semantics and for the convenience of retrieving information. That is not an argument.

The alternative is built into every genome comparison between multiple species. It is a part of the scientific method.

Scientific method relies on directly observed or demonstrated facts, not a priori assumptions.

So why can't a stretch of DNA be from a retrovirus and also have indel mutations? Please explain.

Deleterious effects.

We can directly observe retroviruses producing ERVs in the lab. The ERVs in primate genomes have all of the retroviral genes and features. Why shouldn't we conclude that they came from retroviral insertion?

Again with the 'we', there is no one left LM. I'm going to tell you like I have Papias, they are all gone because the culture wars are over. Now as far as the lab work I'm aware of the Phoenix virus and it can't even be reconstructed. The ERVs are a dead issue and chasing it in circles is a waste of time.

So you are ignoring the evidence that ERVs came from retroviral insertion.

Nope, just bored to death with the circular fallacious logic.

We can observe in the lab how they become permanently fixed in the human genome. They insert into the genome. They are then copied as part of the normal DNA replication of the host genome. Are you really not aware of this?

Again with the we, you are performing in an empty theater.

We can directly observe retroviruses inserting into human genomes. There are several studies where they introduce retroviruses to human cells, and then map the resulting ERVs in the human cells.

http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0020234

You are rummaging a junk yard pretending to pass it off as a viable cause. Unless you are oblivious we are talking about adaptive evolution and I'm really tired of you trying to get me to chase a red herring.

There are over 200,000 ERVs in the chimp genome. Still ignoring this fact?

Are you also still ignoring the fact that the study you are referencing only looked at 425 ERVs?

Officially a dead issue, I think I have been patient enough.

THOSE ARE THE FACTS. I have supported them with scientific references, and yet you refuse to accept these facts because you don't like them. They aren't fabrications. They are facts.

They are a lame homology argument, nothing more. The point of the thread was adaptive evolution not some reading frame graveyard that proves nothing. You don't want to talk about substantive evidence and perform in front of an empty theater be my guest but I'm not going to pretend that it's a real argument.

Have a nice day :)
Mark
 
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mark kennedy

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Anyone else had more than enough of the ersatz ennui on the part of a particular poster?

http://www.flamewarriorsguide.com/warriorshtm/ennui.htm

You got your nerve. Your going to say that because your posts are soooooo interesting. Appreciate the audacity, but without any reference to anything substantive it's more of the same pedantic downward spiral. As long as you have been doing this that's the best you can do. Typical.

Have a nice day :)
Mark
 
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Jimmy D

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There is no dichotomy, the problem is that the only alternative to naturalistic evolution is God, as cause of anything, is rejected a priori (without prior). I don't have a problem with evolution, God doesn't even get credit as designer. Obviously, an a priori assumption of universal common descent going all the way back to, and including, the Big Bang. That's not science, that's supposition.

Have a nice day :)
Mark

Why is it the only alternative? Saying it's either A or B when you have no idea if there could be a C is a blatant false dichotomy. I admit that I haven't followed all your arguments but it seems that they are about specific mechanisms of evolution. Is it not possible that even if you managed to show that these mechanisms didn't work as we understand them to that there could be other naturalistic mechanisms that we haven't yet discovered or understood?

Why do you call common descent an assumption? It's a conclusion drawn from observations, your bias is showing.
 
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VirOptimus

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There is no dichotomy, the problem is that the only alternative to naturalistic evolution is God, as cause of anything, is rejected a priori (without prior). I don't have a problem with evolution, God doesn't even get credit as designer. Obviously, an a priori assumption of universal common descent going all the way back to, and including, the Big Bang. That's not science, that's supposition.

Have a nice day :)
Mark

No, you are quite simply wrong.

Science is a method helping us understand physical reality. Nothing more, nothing less. It is completely neutral on the existance or non-existance of god(s) or any other magical entity.

The physical evidence for evolution and commen descent are very numerous. The ToE is one of the (if not the) best supported theories in science today.

The only reason you reject it is because of your religious beliefs, there is no scientific reason to doubt it.
 
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FrumiousBandersnatch

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The suggestion that anyone claims that the human embryonic structures, that are so reminiscent of the proto-gill slits of fish embryos, were, are, or will be gills, is an obvious (and obviously deliberate) straw man. The structures in the human and fish embryos look similar because they have similar developmental history in the embryo; the same tissue types in the same area developing in similar ways to produce similar structures. In the fish, these structures then develop into gills, in the human, they become parts of the ears and nasopharynx.

The claim is that the structures in the human embryo look similar to the proto-gill slits in the fish embryo because they have been adapted from them to develop into structures other than gills. The same 'repurposing' can be seen in other areas of embryonic development, such as the limb buds and the proto-tail feature. This is just what you'd expect to see if the creatures developed from a common ancestor - the embryonic morphology of the earliest common ancestor developing in different ways in the descendant creatures.
 
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