Is it a hoax?

[mark kennedy]

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

Which is a word that means identical. Sequences prone to mutation won't be. The fact is that the human genome is distinct, and that feature is underscored in this research.

 

[pitabread]

Which is a word that means identical

Huh? Since when does "orthologous" mean identical?

 

[mark kennedy]

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.

For me the fact that they make up some 5–8% of the human genome and what we know about HIV, the scenario is absurd. 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. Them being the result of germline invasions was the deal breaker for me, how many germline invasions into the human genome have been documented in modern times? The HIV invasions into white blood cells are devastating, how much more so germline invasions?

 

[sfs]

Which is a word that means identical.

No, it means that they don't descend from a common ancestral insertion. The identical location is a sign that they're orthologous.

The fact is that the human genome is distinct, and that feature is underscored in this research.

The fact is that ERVs in the same place in multiple species are distributed across species in exactly the way we would expect if they descend from a common ancestor. Why is that, Mark?

 

[sfs]

The HIV invasions into white blood cells are devastating, how much more so germline invasions?

HIV is a close relative of SIV, which infects many monkey species. Guess what kind of effect SIV has on the health of the species that usually carry it. None.

 

[mark kennedy]

No, it means that they don't descend from a common ancestral insertion. The identical location is a sign that they're orthologous.

It assumes common ancestry, suggesting it's a foregone conclusion. Actual proof would be directly connected to actual traits and these are protein coding grave yards.

The fact is that ERVs in the same place in multiple species are distributed across species in exactly the way we would expect if they descend from a common ancestor. Why is that, Mark?

Still dealing with the idea that up to 8% of the human genome is composed of ERVs, the result of germline invasions. That coupled with the fact that CERV 1/PTERV1 is one of the most abundant families of endogenous retroviruses in the chimpanzee genome. That's a lot of germline invasions that simply don't happen except on rare occasions.

 

[mark kennedy]

HIV is a close relative of SIV, which infects many monkey species. Guess what kind of effect SIV has on the health of the species that usually carry it. None.

It's devastating for humans

 

[sfs]

The fact is that ERVs in the same place in multiple species are distributed across species in exactly the way we would expect if they descend from a common ancestor. Why is that, Mark? Why do you never answer that question? Why do genetic data look exactly like common descent is true? That's the case for ERVs, for LINEs, for SINEs, for pseudogenes, for chromosomal rearrangements, for single-base substitutions. Everything looks like common descent is true.

 

[sfs]

It's devastating for humans

So? The point is that not all retroviruses are devastating for the infected species. And different species are more or less susceptible to germ-line invasion at different times. Sooty mangabeys are currently much more likely to have new germ-line insertions than humans.

 

[mark kennedy]

So? The point is that not all retroviruses are devastating for the infected species. And different species are more or less susceptible to germ-line invasion at different times. Sooty mangabeys are currently much more likely to have new germ-line insertions than humans.

Steve seriously, I'm sure this all makes perfect sense to you on some level but higher primates are not mangabeys. This isn't an occasional germline invasion, the Chimpanzee germline would have had to be inundated with them. We are talking about nothing less them a million base pairs since the split. They are rare at the very least and becoming permanently fixed has to be orders of magnitude more unlikely, then add to the fact they have a tendency to remain active. Of course I'm just a novice with an active interest in casual conversation on the subject but if you squint a little, you might see how I'm just a little skeptical.

 

[USincognito]

The Taung Child, that replaced the Piltdown hoax, is a chimpanzee, so is Lucy.

I can't believe Mark is still posting this garbage after all these years.

 

[pitabread]

I can't believe Mark is still posting this garbage after all these years.

I'm not. If there's one thing I've learned about creationist arguments, is that they don't tend to... evolve.

 

[mark kennedy]

The fact is that ERVs in the same place in multiple species are distributed across species in exactly the way we would expect if they descend from a common ancestor. Why is that, Mark? Why do you never answer that question? Why do genetic data look exactly like common descent is true? That's the case for ERVs, for LINEs, for SINEs, for pseudogenes, for chromosomal rearrangements, for single-base substitutions. Everything looks like common descent is true.

For a couple of reasons, not the least of which is that it doesn't explain the requisite adaptive evolution. I don't know why certain places in closely related species have mutations in similar places, I'm not even sure that it matters. The real causation is how you get from a common ancestor and that requires the evolution of brain related genes, why do you never answer those questions?

 

[mark kennedy]

I can't believe Mark is still posting this garbage after all these years.

I can't believe you don't know anything about comparative genetics or the fossil evidence after all these years.

I'm not. If there's one thing I've learned about creationist arguments, is that they don't tend to... evolve.

That's called an ad hominem fallacy, it's like a mutation in your logic.

 

[USincognito]

Did you read this one? 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.

How many times has it been explained to you that the table you keep posting are lineage specific ERVs and does not include the 203,000 shared ERVs that demonstrate common ancestry?

Deleterious effects, starting with SRGAP2.

This is vintage Mark MO, you get introduced to something (in this case by me) and then figure out a way to totally twist or botch what you have learned. In this case it's not just SRGAP2 in a vacuum, but specifically the SRGAP2C allele that is responsible for an increase in the connections in our brains.
Human brain shaped by duplicate genes
>> The team then expressed the human form of SRGAP2C in the neurons of developing mice. The change didn’t cause the mice brains to enlarge, but their neurons produced denser arrays of brain cell structures, called dendritic spines, that forge connections with neighbouring neurons.

“If you’re increasing the total number of connections, you’re probably increasing the ability of this network to handle information,” Polleux says. "It’s like increasing the number of processors in a computer." <<

 

[pitabread]

That's called an ad hominem fallacy, it's like a mutation in your logic.

Everything appears to be an ad hom to you. You're just sensitive.

 

[USincognito]

Ever notice that there are no Chimpanzee ancestors in the fossil record? That’s because every time a gracial (smooth) skull, that is dug up in Asian or Africa they are automatically one of our ancestors.

No, and we've been explaining this to you for ten years now. We don't find chimpanzee fossils because they live in jungles and the acidic soil dissolves bones rather than preserves them. The same goes for many other arboreal species.

 

[mark kennedy]

Everything appears to be an ad hom to you. You're just sensitive.

No actually it's not a complicated formula, the subject me, the predicate something negative with no reference to anything substantive. Your practically addicted to them.

 

[mark kennedy]

How many times has it been explained to you that the table you keep posting are lineage specific ERVs and does not include the 203,000 shared ERVs that demonstrate common ancestry?

The real question is how many times you will try to get me to chase these baseless, irrelevant arguments in circles. I don't know how many we have in common but the ERV class I is the largest most abundant ERVs in the Chimpanzee genome and we don't have any.

This is vintage Mark MO, you get introduced to something (in this case by me) and then figure out a way to totally twist or botch what you have learned. In this case it's not just SRGAP2 in a vacuum, but specifically the SRGAP2C allele that is responsible for an increase in the connections in our brains.
Human brain shaped by duplicate genes
>> The team then expressed the human form of SRGAP2C in the neurons of developing mice. The change didn’t cause the mice brains to enlarge, but their neurons produced denser arrays of brain cell structures, called dendritic spines, that forge connections with neighbouring neurons.

“If you’re increasing the total number of connections, you’re probably increasing the ability of this network to handle information,” Polleux says. "It’s like increasing the number of processors in a computer." <<

The only observed effects of changes in this gene in humans is disease and disorder:

• 15,767 individuals reported by Cooper et al. (2011)] for potential copy-number variation. We identified six large (>1 Mbp) copy-number variants (CNVs), including three deletions of the ancestral 1q32.1 region…
• A ten year old child with a history of seizures, attention deficit disorder, and learning disabilities. An MRI of this patient also indicates several brain malformations, including hypoplasia of the posterior body of the corpus callosum…
• Translocation breaking within intron 6 of SRGAP2A was reported in a five-year-old girl diagnosed with West syndrome and exhibiting epileptic seizures, intellectual disability, cortical atrophy, and a thin corpus callosum. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)

Like all Darwinian arguments, it's an presumed effect without a clue of a cause. We know what happens with mutations, what we have no clue about is the molecular mechanism that makes this happen on such a massive scale.

 

[pitabread]

No actually it's not a complicated formula, the subject me, the predicate something negative with no reference to anything substantive. Your practically addicted to them.

Is pointing out that creationist arguments don't evolve really a 'negative' claim? It's just stating the obvious.

I mean, you guys still gnash your teeth over Piltdown Man. That was a hundred years ago. Let it go already.