Is it a hoax?

[Job 33:6]

Sorry to break it to you @mark kennedy but your arguments aren't making sense. Don't quit your day job!

 

[mark kennedy]

Sure I have. Mutations accumulate after species diverge. That's why the genetic differences between humans and chimpanzees look exactly like lots of accumulated mutations. I know I've pointed that out to you before, too. You didn't have an explanation for it, and you don't seem to care.

I do care but I also know that the vast majority of mutations with effects are deleterious, especially with regards to brain related genes.

I have no idea what that's supposed to mean. As you are quite well aware, I did my bit to determine what the difference was between humans and chimpanzees. The observed difference is, again, quite consistent with being the result of lots of accumulated mutations.

Sure, with regards to single base pairs. But indels are a different matter and some of them are millions of base pairs long. That's a significant number of orders of magnitude are they not.

What obvious problems?

Oh, I don't know, how they happen without frameshifts and major deleterious effects.

You've never understood that genes can be highly conserved under some circumstances and free to evolve under others. (I believe I've also pointed out that HAR1 shows evidence of having been in a high-mutation-rate recombination hotspot, which makes rapid evolution more likely.)

Oh, now you have my complete attention. Do tell, I would be delighted to hear about these mutation hotspots. I would be especially interested in knowing where the data is concerning the effects of mutations in these hotspots.

What problem? They've identified 5000 sites in the genome that have started undergoing transcription. If 1% turned out to be useful, that would not be a shock. Why is it that new genes always turn out to have an obvious mechanistic origin? They're either the result of gene duplication, previously noncoding DNA (which can still be seen in other species), or a transposable element.

I'm not sure what you mean by a 'mechanistic order', because brand new genes require a cause unless I'm completely clueless. The Arctic Cod, I'm sure you remember, did coevolve a gene that created an antifreeze protein no less then four times. It was simple repeats and a brand new gene every time with the same effect. None of these brain related genes are coevolved in humans, how do you explain that? What really puzzles me is when it comes to something as highly conserved brain related genes it's not just a simple protein. This is no cause of concern or even curiosity?

You frequently get facts very wrong. Just in this thread, you've once again gotten the number of ERVs in chimpanzees completely wrong

I never gave a number of ERVs, I cited and quoted a paper you helped write and another paper that said exactly what I quoted and cited and linked.

I like you too, Mark, but you consistently get genetics wrong. I tried, repeatedly, to give you detailed explanations about why you were wrong, but eventually I gave up. Life is too short.

Steve, I just want you to know regardless of what you think of my thoughts on science. You've made a difference, not in my worldview or my thoughts on Creationism but in my understanding of how science actually works. I'm not the sharpest tool in the shed, I know that. But I'm not wrong about how highly conserved genes respond to mutations. All I'm saying is mutations and the rise of highly evolved developmental genes are two different things. They should be treated differently.

Grace and peace,
Mark

 

[xianghua]

No, it isn't Mark. I am saying that common ancestry is evidenced because the distribution of orthologous ERVs matches the expected phylogeny.

not always:

A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans. - PubMed - NCBI

Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans


"It is interesting that one of the three main branches of Old World monkey PTERV1 may actually share a monophyletic origin with the gorilla and chimpanzee elements. One possible scenario may be that this retrovirus was introduced into the great ape lineages by horizontal transmission, perhaps from contact with an ancient Old World monkey specie"

and:

"Second, the PTERV1 phylogenetic tree is inconsistent with the generally accepted species tree for primates, suggesting a horizontal transmission as opposed to a vertical transmission from a common ape ancestor. An alternative explanation may be that the primate phylogeny is grossly incorrect,"

 

[sfs]

not always:

A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans. - PubMed - NCBI

Quite true. Chimpanzees are the species most similar genetically to humans in about two-thirds of the genome. In roughly one-sixth of the genome, we're more closely related to gorillas, and in one-sixth chimpanzees and gorillas are more closely related than either is to humans. This is an expected result with a (relatively) short time between the divergence of gorillas and the human/chimpanzee split. The process is known as incomplete lineage sorting.

Lineage-Specific Expansions of Retroviral Insertions within the Genomes of African Great Apes but Not Humans and Orangutans


"It is interesting that one of the three main branches of Old World monkey PTERV1 may actually share a monophyletic origin with the gorilla and chimpanzee elements. One possible scenario may be that this retrovirus was introduced into the great ape lineages by horizontal transmission, perhaps from contact with an ancient Old World monkey specie"

That's not talking about orthologous ERV insertion points. It's talking about a virus that infected multiple species and inserted into the genomes of each, but in different places. Key sentence: "First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon..."

 

[xianghua]

Quite true. This is an expected result with a (relatively) short time between the divergence of gorillas and the human/chimpanzee split. The process is known as incomplete lineage sorting.

so loudmouth claim that : "distribution of orthologous ERVs matches the expected phylogeny" isnt always true.

That's not talking about orthologous ERV insertion points. It's talking about a virus that infected multiple species and inserted into the genomes of each, but in different places. Key sentence: "First, there is virtually no overlap (less than 4%) between the location of insertions among chimpanzee, gorilla, macaque, and baboon..."

not according to this:

"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates [5]. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"


and still they conclude that this finding contradict the accepted phylogenetic tree. and this is not a single case:

Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats.

"This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past"

 

[Loudmouth]

And you still haven't told me why. You have never acknowledged the genomic divergence with regards to over all genomic divergence, rationalizing away the fact that it's reported at 96% the same at best.

Just stop and think about what you are saying for a moment.

What is evolution? Isn't evolution the process of accumulating mutations over time, resulting in descendants that are modified versions of their ancestors?

Divergence between lineages is exactly what we should see if evolution is true.

Never addressed the obvious problems with the causation regarding gross structural changes in protein coding genes required. No explanation of how HAR1f and the other highly conserved genes suddenly undergo dramatic changes. Then there is the problem with the 60 de novo genes that must have originated some 2 mya. You just keep saying I'm wrong and all I keep doing is reminding you of the facts.

How are evolving genes a problem for evolution?

 

[sfs]

so loudmouth claim that : "distribution of orthologous ERVs matches the expected phylogeny" isnt always true.

They match the actual expectations from the phylogeny, which is surely what's important, right?

not according to this:

"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates [5]. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"


and still they conclude that this finding contradict the accepted phylogenetic tree.

Huh? They found that the vast majority (96%) of insertions were clearly not orthologous. The remaining ones were probably not orthologous either. Those ones don't match the expected phylogeny for the simple reason that they're independent insertions.

this is not a single case:

Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats.

"This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past"

You have again got it wrong. Here they're comparing the phylogeny of the virus with the phylogeny of the primates; they're not looking at the phylogeny suggested by viral insertions. Once again, the conclusions is that the virus moved between species, which is mildly interesting but not at all surprising, since we know viruses do that. They're not reporting anything odd about the viral insertion points.

 

[Loudmouth]

so loudmouth claim that : "distribution of orthologous ERVs matches the expected phylogeny" isnt always true.

It is true with respect to statistical significance.

not according to this:

"We performed two analyses to determine whether these 12 shared map intervals might indeed be orthologous. First, we examined the distribution of shared sites between species (Table S3). We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates [5]. This is particularly relevant for the human/great ape lineage. For example, only one interval is shared by gorilla and chimpanzee; however, two intervals are shared by gorilla and baboon; while three intervals are apparently shared by macaque and chimpanzee. Our Southern analysis shows that human and orangutan completely lack PTERV1 sequence (see Figure 2A). If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely"


and still they conclude that this finding contradict the accepted phylogenetic tree. and this is not a single case:

If you read further into the paper you will find this:

For the three intervals putatively shared between macaque and chimpanzee, we attempted to refine the precise position of the insertions by taking advantage of the available whole-genome shotgun sequences for these two genomes. For each of the three loci, we mapped the precise insertion site in the chimpanzee and then examined the corresponding site in macaque (http://www.ncbi.nlm.nih.gov). In one case, we were unable to refine the map interval owing to the presence of repetitive rich sequences within the interval. In two cases, we were able to refine the map location to single basepair resolution (Figures S4 and S5). Based on this analysis, we determined that the sites were not orthologous between chimpanzee and macaque. It is interesting to note that this level of refined mapping in chimpanzee revealed 4- to 5-bp AT-rich target site duplications in both cases. These findings are consistent with an exogenous retrovirus source since proviral integrations typically target AT-rich DNA ranging from 4 to 6 bp in length [24]. Although the status of the remaining overlapping sites is unknown, these data resolve four additional sites as independent insertion events and suggest that the remainder may similarly be non-orthologous.​

They were unable to find a single unambiguous orthologous PtERV insertion that violated the expected phylogeny.

Distribution of baboon endogenous virus among species of African monkeys suggests multiple ancient cross-species transmissions in shared habitats.

"This viral evolutionary tree does not follow host phylogeny, indicating the cross-species transmissions and multiple germ line fixations of the virus must have occurred in the past"

That is referring to the evolution of the virus, not the primate species. They are talking about the viral DNA sequence itself, not their placement in the host genome.

 

[sfs]

No, I'm offering to have a serious, honest, adult discussion with you about why evolution explains the diversity of life.

Maybe he didn't want a serious discussion after all.

 

[lesliedellow]

Maybe he didn't want a serious discussion after all.

What a surprise.

 

[xianghua]

Those ones don't match the expected phylogeny for the simple reason that they're independent insertions.

but they actually do talking about shared sites:

"First, we examined the distribution of shared sites between species (Table S3)"

and their conclusion:

"We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"

 

[sfs]

but they actually do talking about shared sites:

"First, we examined the distribution of shared sites between species (Table S3)"

and their conclusion:

"We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"

Oh for crying out loud. These are sites that we've already discussed, ones that mapped to more or less the same part of the genome but that couldn't be definitively shown to be in the same or different spots. The authors are quite explicit: "Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) and could not be definitively resolved as orthologous or non-orthologous (Table S3)." Why didn't you quote that bit? Or the title of the Table S3, "Retroviral Map Intervals That Potentially Overlap between Species"? What do you think "potentially" means in that title?

At this point in the paper, they've already shown that 96% of insertions did not occur in the same place in the different species. These 24 are the remaining 4%. When they looked at some of these in more detail, they showed that 4 were not orthologous: "Although the status of the remaining overlapping sites is unknown, these data resolve four additional sites as independent insertion events and suggest that the remainder may similarly be non-orthologous." So they have provided no reason to think any of the remaining 20 insertions actually occur in orthologous locations, and no reason to think there's anything here that violates the phylogeny.

The whole paper is good evidence for the validity of the phylogeny, not evidence against it.

 

[mark kennedy]

Just stop and think about what you are saying for a moment.

What is evolution? Isn't evolution the process of accumulating mutations over time, resulting in descendants that are modified versions of their ancestors?

No, it's the change of alleles in population over time, mutations are irrelevant.

Divergence between lineages is exactly what we should see if evolution is true.

Extinction is what we would expect to see if all evolution is, is the accumulation of genetic mutations.

How are evolving genes a problem for evolution?

An effect without a cause isn't science, it's supposition.

 

[mark kennedy]

but they actually do talking about shared sites:

"First, we examined the distribution of shared sites between species (Table S3)"

and their conclusion:

"We found that the distribution is inconsistent with the generally accepted phylogeny of catarrhine primates"

Yea and then there is this:

If these sites were truly orthologous and, thus, ancestral in the human/ape ancestor, it would require that at least six of these sites were deleted in the human lineage. Moreover, the same exact six sites would also have had to have been deleted in the orangutan lineage if the generally accepted phylogeny is correct. Such a series of independent deletion events at the same precise locations in the genome is unlikely.
​

This underscores the divergence of humans from apes. Good luck getting them to admit it.

 

[Astrophile]

Still waiting for some atheist to tell me what evolved first DNA or Protein , I asked once my bio teacher and he was bullying me for rest of year .

Why is it important to know which evolved first?

 

[xianghua]

Oh for crying out loud. These are sites that we've already discussed, ones that mapped to more or less the same part of the genome but that couldn't be definitively shown to be in the same or different spots. The authors are quite explicit: "Within the limits of this BAC-based end-sequencing mapping approach, 24 sites mapped to similar regions of the human reference genome (approximately 160 kb) .

even if those ervs are in a similar spot in the genome and not identical, it's almost the same. what is the chance that in a 3bilion bp we will get the same ervs in a tiny spots in that genome?

another point is the unique ervs. if human have about 100 unique non functional ervs, and a fixation time for a neutral mutation is about 1 my in a small population, then it will take about 100my to get 100 unique ervs. so those ervs may be functional. and if they are functional then it's a good evidence that they are the result of design and not evolution.

 

[sfs]

This underscores the divergence of humans from apes. Good luck getting them to admit it.

No, it underscores the fact that the insertions really aren't orthologous.

 

[Astrophile]

It is interesting to know that Darwin, in later life, regretted writing his book and said that his theory was "the unborn idea of a young man." If that is what the founder of Evolution said, then that must put a bit of dent in it.

In fact Darwin (1809-82) was 50 when The Origin of Species was published (November 1859).

 

[sfs]

In fact Darwin (1809-82) was 50 when The Origin of Species was published (November 1859).

Also, Google: 'No results found for "unborn idea of a young man".'

 

[sfs]

even if those ervs are in a similar spot in the genome and not identical, it's almost the same. what is the chance that in a 3bilion bp we will get the same ervs in a tiny spots in that genome?

The spots aren't that tiny; they're ~160,000 bp in size. Yes, we would only expect independent insertions in the same region very rarely -- if insertion probability is uniform across the genome. Since retroviruses and transposons both tend to have substantial biases in what parts of the genome they insert into, however, we shouldn't have any particular expectation of how clustered these insertion points should be. To tell that, you'd have to do a detailed analysis of insertion biases for this virus. Have you done that?

In any case, I have no idea what you're trying argue at this point. Common descent makes strong predictions about ERV insertions into identical locations in different species: they should follow the phylogeny (with the usual qualifications about things like incomplete lineage sorting). They do. Common descent makes no prediction about ERV insertions that aren't in identical locations, whether they're 10 bp apart or 10 million bp. So what is this supposed to be evidence of?