Chimpanzee Genome

[mark kennedy]

I spend most of my time in the Origins Theology forum but theistic evolutionists have little patience of reading scientific literature. I think the reason must be that you think very differently about science then you do religion. Which makes it hard to get them into the details of something as intricate as Genomics. I have also promised LM a discussion of ERVs that he considers a virtual smoking gun for Chimpanzee/Human common ancestry. At any rate, the purpose of the thread is to take up the subject of comparative genomics.

There is a standard line in the Darwinian theater of the mind that we are 98% the same as the Chimpanzee in our DNA. The scientific world has known for some time that this isn't true but you still keep seeing this in their popular press.

The fact is that we are not 98% the same in our DNA:

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 (Nature, 1 September 2005)​

The paper cites these references:

• Britten, R. J. Divergence between samples of chimpanzee and human DNA sequences is 5%, counting indels. Proc. Natl Acad. Sci. (2002)
• Frazer, K. A. et al. Genomic DNA insertions and deletions occur frequently between humans and nonhuman primates. Genome Res. (2003)
• Locke, D. P. et al. Large-scale variation among human and great ape genomes determined by array comparative genomic hybridization. Genome Res. (2003)
• Liu, G. et al. Analysis of primate genomic variation reveals a repeat-driven expansion of the human genome. Genome Res. 13, (2003)
• Yohn, C. T. et al. Lineage-specific expansions of retroviral insertions within the genomes of African great apes but not humans and orangutans. PLoS Biol. (2005)

It is puzzling that the announcement of the article would make this obviously bogus statement:

What makes us human? We share more than 98% of our DNA and almost all of our genes with our closest living relative, the chimpanzee. (Nature, Web Focus)​

Loudmouth and I had been debating and discussing for some time when I finally talked him into a formal debate. The formal debate thread had been started and I was itching to put it to good use. Most evolutionists would not dare let a creationist get then on record, losing a debate with a creationist would be academic suicide. Casual discussion boards is another matter. At any rate, the discussion of ERVs can be found here:

mark kennedy v. Loudmouth

It's an homology argument, basically it says that because we are so similar we must have a common ancestor. The subject matter was new to me so I thought I was going to have to do a lot of reading but the refutation was shockingly easy to find:

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.

Ok, I know what your thinking, who care about difference in junk DNA right? What about protein coding genes? 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). Genome wide the differences are now known to include 35 million single base substitutions, and five million indels (with the ~70,000 indels larger than 80 bp comprising 73% of the affected base pairs). This is in addition to 8 chromosomal rearrangements from 2 million base pairs to 4 million base pairs in length coming to more then 20 million base pairs.

Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives. (The Evolution of Mammalian Gene Families)​

One has to wonder what the mutation rate would have to be in order to get this kind of divergence. I expected a formula something like this one:

Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.


Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
-----------------------------------------------------

Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000)​

For reasons I can't quite grasp no evolutionist will touch the mutation rate with a ten foot pole. Now I managed to talk an MIT staff scientist into showing the rate for single base substitutions but they avoid the indels like the plague.

This is the one that sealed the deal for me. This one staggers the imagination and evolutionists literally have no clue how it could have happened:

The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 myr ago​

Here's how it breaks down Barney style. For 400 million years this gene allows only 2 substitutions. In the lineage that became human it allows 18, how is this even conceivable, never mind possible and it is certainly not explained.

The thread is about homology arguments as they relate to comparative genomics. Like I said, I promised LM I would discuss the ERVs with him when I got some time and I think I can manage it now. Usually when I bring the subject up the average troll will avoid the thread like the plague, they are just not capable of doing this kind of technical reading. They lose the tag team effect which is their support system so they just peel off one by one.

Be advised I will not fall prey to fallacious circular arguments so if that's all you have don't blame me when you get your feeling hurt. I only mention that because I know what the trolling tactics are like on here and I don't want the novice trollers to get caught up in the mix. It is not my intention to discourage people with an interest in evolutionary biology to shy away from the scientific literature. On the contrary, I think these forums could go a long way to improve the ability of the layman to navigate these highly technical publications.

That's by no means an exhaustive sampling of the subject matter but you'll probably have to agree that it's a little more technical then the average thread on here. I also want to add that if you are a Christian who has embraced theistic evolution I'm perfectly willing to discuss the doctrinal and theological issues but I would rather do that in another thread, preferably in the Origins Theology forum.

Grace and peace,
Mark

 

[sfs]

I
That's by no means an exhaustive sampling of the subject matter but you'll probably have to agree that it's a little more technical then the average thread on here. I also want to add that if you are a Christian who has embraced theistic evolution I'm perfectly willing to discuss the doctrinal and theological issues but I would rather do that in another thread, preferably in the Origins Theology forum.

To me it looks like a rehash of every misunderstanding of genetics you've ever posted here. Not exactly an exciting menu.

 

[Tomk80]

To me it looks like a rehash of every misunderstanding of genetics you've ever posted here. Not exactly an exciting menu.

^this^

 

[mark kennedy]

To me it looks like a rehash of every misunderstanding of genetics you've ever posted here. Not exactly an exciting menu.

That's just a primer, where would you like to take the thread to make it more substantive?

^this^

What?

 

[Loudmouth]

There is a standard line in the Darwinian theater of the mind that we are 98% the same as the Chimpanzee in our DNA.

What are the units of the comparison?

It's an homology argument, basically it says that because we are so similar we must have a common ancestor.

The argument, specifically, was that 200,000 ERV's found at the same position in both humans and chimps could only be explained by common ancestry:

First, the distribution of provirus-containing loci among taxa dates the insertion. 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).
Constructing primate phylogenies from ancient retrovirus sequences
​

We have 200,000 such ERV insertions shared with chimps.

The subject matter was new to me so I thought I was going to have to do a lot of reading but the refutation was shockingly easy to find:

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).

And there is the bait and switch.

Those ERV's listed are the ones that are not shared. They are a tiny, tiny percentage of the 200,000 that are shared. In humans, all but 82 of the 200,000 ERV's are shared with chimps. In chimps, all but 279 of the 200,000 ERV's areare shared with humans.

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.
Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses

​

So they looked at just 425 out of 200,000 ERV's, and from that Mark thinks that PtERV1 insertions are still the most numerous in the genome. Yeah, right.

Ok, I know what your thinking, who care about difference in junk DNA right? What about protein coding genes? 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.

What was the average difference between those genes? Here is a question for you. Tell me the % homology between these two sequences, and how many mutations produced these changes:

Sequence A: AATATT----GTTCCTAGG
Sequence B: TATATTTATTGTTCCTAGG

 

[MrsLurking]

I spend most of my time in the Origins Theology forum but theistic evolutionists have little patience of reading scientific literature.

Yes, Dr. Francis Collins and I are both theistic evolutionists and scientists who are weak on reading the scientific literature.

(Exaggerate and generalize much?)

 

[MrsLurking]

I
There is a standard line in the Darwinian theater of the mind that we are 98% the same as the Chimpanzee in our DNA.

The overall statistic is interesting but is not at all necessary to establish the fact that genome mapping was yet another slam-dunk confirmation of the theory of evolution. The raw data statistics are not nearly as important as the underlying NESTED HIERARCHIES of the details.

Genomics was yet another grand test of the ToE. It could have FALSIFIED the theory----but it didn't. It not only confirmed it, it demonstrated that the predictions of genomic sequences published years before based on the ToE were dead-on correct!

So you can argue percentages all you wish. It is the nested hierarchies clearly displayed in the mapping that devastates your ill-informed claims.

Praise God for his amazing evolutionary processes! Modern day Pharisees will continue to do just what their first century counterparts did: They observed the wondrous works of God and attributed them to Satan! It was blasphemy then and it is blasphemy now.

 

[sfs]

That's just a primer, where would you like to take the thread to make it more substantive?

None of our threads have ever become substantive that I can recall. As Loudmouth's post illustrates, you frequently don't understand the data you're using (even when, as in this case, it's been explained to you repeatedly). That makes serious engagement with the substantive issues impossible.

 

[Loudmouth]

One has to wonder what the mutation rate would have to be in order to get this kind of divergence. I expected a formula something like this one:

Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.


Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
-----------------------------------------------------

Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000)
​

For reasons I can't quite grasp no evolutionist will touch the mutation rate with a ten foot pole. Now I managed to talk an MIT staff scientist into showing the rate for single base substitutions but they avoid the indels like the plague.

This is the one that sealed the deal for me. This one staggers the imagination and evolutionists literally have no clue how it could have happened:

The 118-bp HAR1 region showed the most dramatically accelerated change, with an estimated 18 substitutions in the human lineage since the human–chimpanzee ancestor, compared with the expected 0.27 substitutions on the basis of the slow rate of change in this region in other amniotes. Only two bases (out of 118) are changed between chimpanzee and chicken, indicating that the region was present and functional in our ancestor at least 310 million years (myr) ago. No orthologue of HAR1 was detected in the frog (Xenopus tropicalis), any of the available fish genomes (zebrafish, Takifugu and Tetraodon), or in any invertebrate lineage, indicating that it originated no more than about 400 myr ago
​

This is another example of a bait and switch. First, Mark talks about the divergence of selectively neutral sites, and then immediately switches to a site under strong positive selection without telling the reader. Either this is purposeful lying, or Mark doesn't know what he is talking about. Either way, it doesn't cast Mark in a positive light, especially given the fact that these errors have been pointed out to him before.

 

[MrsLurking]

This is another example of a bait and switch. First, Mark talks about the divergence of selectively neutral sites, and then immediately switches to a site under strong positive selection without telling the reader. Either this is purposeful lying, or Mark doesn't know what he is talking about. Either way, it doesn't cast Mark in a positive light, especially given the fact that these errors have been pointed out to him before.

He doesn't have a clue. I especially enjoyed this excerpt from Mark's remarks:

>"For reasons I can't quite grasp no evolutionist will touch the mutation rate with a ten foot pole."
​

Not only can't he grasp the concept, he didn't bother to check the peer-reviewed literature to see that they talk about mutation rates all the time. Thus, are the dangers of blind copy-and-paste from creationist websites.

"Now I managed to talk an MIT staff scientist into showing the rate for single base substitutions but they avoid the indels like the plague."


​

Did you ever notice that evolution-deniers always seem to be talking to MIT or UCLA scientists or professors who always remain nameless and make shocking or embarassing statements which we have no way to track down? Convenient hearsay anyopne?

Pathetic.

 

[sfs]

[/I][/INDENT]Did you ever notice that evolution-deniers always seem to be talking to MIT or UCLA scientists or professors who always remain nameless and make shocking or embarassing statements which we have no way to track down? Convenient hearsay anyopne?

Pathetic.

I assume he's talking about me (although I'm more affiliated with Harvard than with MIT lately).

 

[MrsLurking]

I assume he's talking about me (although I'm more affiliated with Harvard than with MIT lately).

I mentioned it this trend because Kent Hovind, Ray Comfort, and Lee Strobel (and probably many others) have popular anecdotes they use in their lectures which refer to unnamed professors at various top institutions who they happened to talk with on some flight or radio call-in program. Kent Hovind has his imaginary Berkeley professor who, strangely enough, uses the same strawman descriptions of evolution that Hovind uses!

 

[mark kennedy]

What are the units of the comparison?

Base pairs obviously.

The argument, specifically, was that 200,000 ERV's found at the same position in both humans and chimps could only be explained by common ancestry:

First, the distribution of provirus-containing loci among taxa dates the insertion. 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).
Constructing primate phylogenies from ancient retrovirus sequences​

Your source material is from 1999 LM, I don't disagree with the conclusion if the premise is sound. But then you jump to this conclusion:

We have 200,000 such ERV insertions shared with chimps.

That's from the original Human Genome paper and there was no Chimpanzee Genome to compare it to until 2005. Your begging the question of proof again but let's see where you go with this.

And there is the bait and switch.

Those ERV's listed are the ones that are not shared. They are a tiny, tiny percentage of the 200,000 that are shared. In humans, all but 82 of the 200,000 ERV's are shared with chimps. In chimps, all but 279 of the 200,000 ERV's areare shared with humans.

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.
Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses​

There are a couple of problems with this. First of all 7% of the divergence is because of ERVs, that pretty much nullifies any bogus claim that they are all virtually identical. Most importantly

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)​

So the ERVs are virtually identical but 7% of the divergence is from them and the single most abundant family of ERVs is absent in the human genome:

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. (Nature, 2005)​

This is most likely the worst homology argument I have ever seen. I can't believe you are still buying into this stuff.

We report here that the chimpanzee genome contains at least 42 separate families of endogenous retroviruses, nine of which were not previously identified. All but two (CERV 1/PTERV1 and CERV 2) of the 42 families of chimpanzee endogenous retroviruses were found to have orthologs in humans. Molecular analysis (PCR and Southern hybridization) of CERV 2 elements demonstrates that this family is present in chimpanzee, bonobo, gorilla and old-world monkeys but absent in human, orangutan and new-world monkeys. A survey of endogenous retroviral positional variation between chimpanzees and humans determined that approximately 7% of all chimpanzee-human INDEL variation is associated with endogenous retroviral sequences. Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses​

So they looked at just 425 out of 200,000 ERV's, and from that Mark thinks that PtERV1 insertions are still the most numerous in the genome. Yeah, right.

So far you have not qualified that statement. Why don't you do a little reading and give us all an accurate accounting of just how many ERVs there are in the Human Genome, the Chimpanzee Genome and then we can make an accurate comparison. The Talk Origins article that you got this argument from said that ERVs make up 1% of the human genome, we now know that it's more like 8%.

Retroelements and the human genome: New perspectives on an old relation


After all this time you are still confused about the facts.

What was the average difference between those genes? Here is a question for you. Tell me the % homology between these two sequences, and how many mutations produced these changes:

Sequence A: AATATT----GTTCCTAGG
Sequence B: TATATTTATTGTTCCTAGG

Ok, I will do that for you if you'll do something for me. When the divergence goes from 1.3% to 6%, what is the mutation rate?

This is the table based on 1.33% divergence:

---------------------------------------------------
Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.


Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
-----------------------------------------------------

Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000)​

When the actual divergence is found to be between 5% and 6% does the calculation of the mutation rate change?

 

[mark kennedy]

Yes, Dr. Francis Collins and I are both theistic evolutionists and scientists who are weak on reading the scientific literature.

(Exaggerate and generalize much?)

Francis Collins doesn't post here much, as a matter of fact, I would be interested in seeing how he explains the divergence.

 

[Loudmouth]

Base pairs obviously.

Really? Then why do you switch to genes as your unit of comparison later in your post? Also, how are indels counted as part of the comparison, or are they?

Your source material is from 1999 LM, I don't disagree with the conclusion if the premise is sound. But then you jump to this conclusion:



That's from the original Human Genome paper and there was no Chimpanzee Genome to compare it to until 2005. Your begging the question of proof again but let's see where you go with this.

Why do you need to compare the human genome to the chimp genome in order to count the number of ERV's in the human genome? The answer is you don't. They counted 200,000 ERV's in the human genome. It's right there in the human genome paper.

When they sequenced the chimp genome they used the same technique to find all of the ERV's in the chimp genome. They then compared the position and sequence of the two sets and determined which were not shared. As it turns out, less than 100 human ERV's are specific to humans and less than 300 are specific to chimps. The other 99.99% of the 200,000 ERV's are at the same location in each genome. Those are the facts you keep running away from.

There are a couple of problems with this. First of all 7% of the divergence is because of ERVs, that pretty much nullifies any bogus claim that they are all virtually identical.

Again, you are running away from the facts.

Most importantly

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)​

​

The authors of that paper only looked at 425 ERV's which is just 0.02% of the total number of ERV's. Yes, they were the most abundant of the 0.02% of the ERV's they looked at, but to extrapolate that to the 99.98% of the rest of the ERV's is well beyond what the data will allow.

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. (Nature, 2005)
This is most likely the worst homology argument I have ever seen. I can't believe you are still buying into this stuff.

99.99% of ERV's are orthologous between humans and chimps. Why is that the worst homology argument ever? Please explain.

Also, please explain why PtERV1 elements are found at non-orthologous positions amongst apes just as evolution predicts.

We report here that the chimpanzee genome contains at least 42 separate families of endogenous retroviruses, nine of which were not previously identified. All but two (CERV 1/PTERV1 and CERV 2) of the 42 families of chimpanzee endogenous retroviruses were found to have orthologs in humans. Molecular analysis (PCR and Southern hybridization) of CERV 2 elements demonstrates that this family is present in chimpanzee, bonobo, gorilla and old-world monkeys but absent in human, orangutan and new-world monkeys. A survey of endogenous retroviral positional variation between chimpanzees and humans determined that approximately 7% of all chimpanzee-human INDEL variation is associated with endogenous retroviral sequences. Identification, characterization and comparative genomics of chimpanzee endogenous retroviruses

And none of them are found at orthologous positions, just as the theory of evolution predicts. More evidence for my side.

So far you have not qualified that statement. Why don't you do a little reading and give us all an accurate accounting of just how many ERVs there are in the Human Genome, the Chimpanzee Genome and then we can make an accurate comparison.

Already have. The human genome paper reports 200,000 ERV's in the human genome across three classes:

Table 11 : Initial sequencing and analysis of the human genome : Nature

Of those, less than 100 are found only in humans as your table from the chimp genome paper discusses. Of those found in the chimp, less than 300 are found only in the chimp with the other 200,000 found at the same location in humans.

The Talk Origins article that you got this argument from said that ERVs make up 1% of the human genome, we now know that it's more like 8%.

Then don't use the Talk Origins number that was based on incomplete data.

Ok, I will do that for you if you'll do something for me. When the divergence goes from 1.3% to 6%, what is the mutation rate?

You can not determine the mutation rate from divergence in sequences that are under selective pressure. Rule #1 for molecular clocks.

 

[mark kennedy]

He doesn't have a clue. I especially enjoyed this excerpt from Mark's remarks:

>"For reasons I can't quite grasp no evolutionist will touch the mutation rate with a ten foot pole."
​

Not only can't he grasp the concept, he didn't bother to check the peer-reviewed literature to see that they talk about mutation rates all the time. Thus, are the dangers of blind copy-and-paste from creationist websites.

"Now I managed to talk an MIT staff scientist into showing the rate for single base substitutions but they avoid the indels like the plague."


​

Did you ever notice that evolution-deniers always seem to be talking to MIT or UCLA scientists or professors who always remain nameless and make shocking or embarassing statements which we have no way to track down? Convenient hearsay anyopne?

Pathetic.

They do avoid the indels like the plague but they have no clue how the ones that would have had to occur in the human genome since the split could have happened.

What is more not once has an evolutionist explained the HAR1f gene. For 400 million years this highly conserved gene allows only 2 substitutions then all of the sudden it allows 18. Let me clue you in, I don't get my information from Creationist websites. I get my information from the actual scientific literature and it requires no great amount of knowledge to see the obvious. Beneficial effects from mutations in the human brain don't happen, much less on an evolutionary scale.

When there is a mutation in a brain related gene you get a deleterious (harmful) effect, every single time. Beneficial effects from mutations do happen but not in the single greatest evolutionary giant leap in our lineage. How did they get there in the first place?

Nice to see the trolls are still hanging in there. This would be a dead thread without them.

Have a nice day
Mark

 

[Loudmouth]

They do avoid the indels like the plague . . .

The only reason you know what the indel numbers are is because they reported them and discussed them. Why do we need to avoid the indels? Please explain.

When there is a mutation in a brain related gene you get a deleterious (harmful) effect, every single time. Beneficial effects from mutations do happen but not in the single greatest evolutionary giant leap in our lineage. How did they get there in the first place?

Empty assertions. You need evidence to back this up.

 

[Notedstrangeperson]

As the other users have pointed out, several of the points OP makes (such as whether humans and apes really share 98% of their DNA and whether the presence of ERVs are an indicator of ancestry) have already been discussed - and refuted.

Mark Kennedy does make one interesting point though...

One has to wonder what the mutation rate would have to be in order to get this kind of divergence.

Recently it has been thought that humans and chimps may have diverged earlier than previously estimated. The general consensus is between 6 to 7 million years ago. However some now push that back to an incredible 14 million years ago:

Langergraber et al. (2012) note that comparatively little has been done to improve our knowledge of ape generation length. No matter how accurate our figures regarding mutations are, the resulting date of divergence will still be wrong if we don’t have a good understanding of how long generations are.

So Langergraber et al. (2012) went and documented the ages of parents in ape communities in an effort to identify the length of each generation. Their results pushed back the chimp generation length from the previously identified 22 years to 25 years, the gorilla generation shortened from 20 years to 19 years and the human generation length went up from 25 years to 29 years.

Taken together these figures effectively double our previous divergence dates. Humans and chimps now split between 7 – 14 million years ago; humans and Neanderthals split ~600 – 800,000 years ago and humans began to migrate across the globe ~100,000 years ago. These figures are truly revolutionary, forcing us to reconsider how we view many fossils.

theadvancedapes.com​

That said, the original study (Langergraber et al. (2012) does have a lower estimate of 7 million years, which as the author says would fit in with both molecular estimates and fossil findings.

Nevertheless, it seems odd to have such an enormous gap - one that is more than double the original estimate. Though I personally am a little skeptical (since this study looked at generation lengths rather than genetics), I suppose it could explain why humans have accumulated a great deal of mutations is seemingly such a short amount of time - because it wasn't such a "short" amount of time after all.

This may also force us to reconsider certain fossils - fossils which despite having seemingly "human" features (such as Oreopithecus and Anoiapithecus) are not considered hominids because they were too old.

 

[mark kennedy]

Really? Then why do you switch to genes as your unit of comparison later in your post? Also, how are indels counted as part of the comparison, or are they

The indels are simply gaps, differences of length. Of course they are counted unless they don't fit one of these homology arguments, then they are ignored.

Why do you need to compare the human genome to the chimp genome in order to count the number of ERV's in the human genome? The answer is you don't. They counted 200,000 ERV's in the human genome. It's right there in the human genome paper.

Right, but they are not 1% of the human genome they are 8%. Did they grow in length over the five years it took for the revision to finally emerge? Of course you need a Chimpanzee Genome to compare them to otherwise you are making a false assumption that they are actually the same.

When they sequenced the chimp genome they used the same technique to find all of the ERV's in the chimp genome. They then compared the position and sequence of the two sets and determined which were not shared. As it turns out, less than 100 human ERV's are specific to humans and less than 300 are specific to chimps. The other 99.99% of the 200,000 ERV's are at the same location in each genome. Those are the facts you keep running away from.

The PERVs are the most abundant family of ERVs and make up 7% of the divergence. That is a fact you are not running away from but obviously unaware of. Your not making an actual comparison, your just throwing numbers out there and pretending they are accurate. How many base pairs total are the ERVs in the Human and Chimpanzee Genomes and what percent of the respective genomes do the ERVs represent?

Again, you are running away from the facts.

So far you haven't manage to substantiate any of them.

The authors of that paper only looked at 425 ERV's which is just 0.02% of the total number of ERV's. Yes, they were the most abundant of the 0.02% of the ERV's they looked at, but to extrapolate that to the 99.98% of the rest of the ERV's is well beyond what the data will allow.

I've seen how you 'extrapolate' and it's bogus. So far you have failed to substantiate that claim, or even attempt to.

99.99% of ERV's are orthologous between humans and chimps. Why is that the worst homology argument ever? Please explain.

Because it's not true.

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).​

You have never managed to answer that point.

Also, please explain why PtERV1 elements are found at non-orthologous positions amongst apes just as evolution predicts.

It doesn't matter, your trailing off on irrelevant details

And none of them are found at orthologous positions, just as the theory of evolution predicts. More evidence for my side.

Orthologous simple means the same. Yea, I can see how that would appeal to someone making an homology argument but it's a random argument.

Already have. The human genome paper reports 200,000 ERV's in the human genome across three classes:

Table[bless and do not curse]11 : Initial sequencing and analysis of the human genome : Nature

No, you have a dated list that shows ERVs are 1% of the human genome, they percentage has jumped up to 8%. Don't think your source material is reliable.

Of those, less than 100 are found only in humans as your table from the chimp genome paper discusses. Of those found in the chimp, less than 300 are found only in the chimp with the other 200,000 found at the same location in humans.

That's what you keep saying based on dated material and false assumptions. At least 7% of the divergence between us and Chimpanzees is due to these ERVs and you would have me believe that they are virtually all identical. It's absurd.

Then don't use the Talk Origins number that was based on incomplete data.

It's based on the same source material you are still using.

You can not determine the mutation rate from divergence in sequences that are under selective pressure. Rule #1 for molecular clocks.

Don't need a molecular clock, need a mutation rate.

 

[mark kennedy]

As the other users have pointed out, several of the points OP makes (such as whether humans and apes really share 98% of their DNA and whether the presence of ERVs are an indicator of ancestry) have already been discussed - and refuted.

No it hasn't, I stopped posting here because they didn't want to admit that the claim that we are 98% the same in our DNA is wrong. If you think this point has been refuted suppose you tell me, are we 98% the same as Chimpanzees in our DNA or not? The ERVs are not really proof of anything but they are not identical in the two genomes, in fact, the single most abundant family of ERVs is absent in the human genome. Neither of these points have been refuted because they can't be.

Mark Kennedy does make one interesting point though...

Recently it has been thought that humans and chimps may have diverged earlier than previously estimated. The general consensus is between 6 to 7 million years ago. However some now push that back to an incredible 14 million years ago:

Langergraber et al. (2012) note that comparatively little has been done to improve our knowledge of ape generation length. No matter how accurate our figures regarding mutations are, the resulting date of divergence will still be wrong if we don’t have a good understanding of how long generations are.

So Langergraber et al. (2012) went and documented the ages of parents in ape communities in an effort to identify the length of each generation. Their results pushed back the chimp generation length from the previously identified 22 years to 25 years, the gorilla generation shortened from 20 years to 19 years and the human generation length went up from 25 years to 29 years.

Taken together these figures effectively double our previous divergence dates. Humans and chimps now split between 7 – 14 million years ago; humans and Neanderthals split ~600 – 800,000 years ago and humans began to migrate across the globe ~100,000 years ago. These figures are truly revolutionary, forcing us to reconsider how we view many fossils.

theadvancedapes.com​

That said, the original study (Langergraber et al. (2012) does have a lower estimate of 7 million years, which as the author says would fit in with both molecular estimates and fossil findings.

Yea that's the famous trick of Darwinism, when you can't explain it just move the date back. There's one major problem with that, we don't have any chimpanzee ancestors in the fossil record for 25 million years. The ERVs, BTW, for the most part go back about 25 million years ago. I really don't know what moving the date back does for you but it looks like the only way to explain the divergence to me.

Nevertheless, it seems odd to have such an enormous gap - one that is more than double the original estimate. Though I personally am a little skeptical (since this study looked at generation lengths rather than genetics), I suppose it could explain why humans have accumulated a great deal of mutations is seemingly such a short amount of time - because it wasn't such a "short" amount of time after all.

This may also force us to reconsider certain fossils - fossils which despite having seemingly "human" features (such as Oreopithecus and Anoiapithecus) are not considered hominids because they were too old.

This is the only problem I think evolutionists should be concerned with, when and how did this happen?

FIGURE 2. Comparative neuroanatomy of humans and chimpanzees. (Genetics and the making of Homo sapiens. Nature April 2003)