Is it a hoax?

mark kennedy

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Actually, one of the groups of genes that experience the most mutations in the human genome are related to brain growth and development.

Brain related genes aren't highly conserved; I feel like we have had this discussion before. HOX genes, genes that signal structures to develop in certain spots, are highly conserved and thus present in very similar forms even in organisms not closely related, such as between fruit flies and humans. But, as for brain genes in general, in humans, they are some of the most frequently mutating genes. The overall super high mutation rate in our species could be to blame for our high rate of miscarriage.[/quote]

I see nothing good coming from mutations in the HOX genes and a Pandora's box of deleterious effects:

  • HOXA1 Bosley–Salih–Alorainy syndrome (BSAS) Athabascan brainstem dysgenesis syndrome (ABDS)
  • HOXA2-associated autosomal recessive microtia
  • ARX (the aristaless-related homeobox gene) is a transcription factor that participates in the development of GABAergic and cholinergic neurons in the forebrain. Many ARX mutations have been identified in X-linked lissencephaly and mental retardation with epilepsy (Hum Mol Genet. 2009 Oct 1)

The reason why being bipedal is a strong argument against an organism being an ancestor to chimpanzees is because the bipedal trait appeared long after the human and chimp lineage split and is present in the human lineage. Since chimps aren't bipedal and split off from the lineage that has said trait before the trait appeared, it wouldn't make any sense for chimps to have any bipedal ancestors. Same goes for smaller teeth.
So it makes little sense that the chimpanzee at one time was bipedal but it makes perfect sense that highly conserved brain related genes can undergo massive overhauls and de novo creation?
 
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tas8831

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The change of alleles happen a lot of different ways, the CRISPR gene no one has the slightest interest in is one way bacteria adapted the immune system.

Already told you that CRISPR is not a gene.
There is exon shuffling and various epigenetic ways of this happening. Virtually none of them apply to highly conserved brain related genes.

So what?

Do you think that there is a 1-to-1 relationship between mutations and phenotype (or even genes to phenotype, for that matter)?

You keep refusing to answer this.
 
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mark kennedy

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Already told you that CRISPR is not a gene.

I must of missed that or is this just a pedantic distraction because you seem to like those. Irrelavant corrections seem to be your forte.

So what?

Do you think that there is a 1-to-1 relationship between mutations and phenotype (or even genes to phenotype, for that matter)?

You keep refusing to answer this.

It depends on the mutation
 
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tas8831

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I must of missed that or is this just a pedantic distraction because you seem to like those. Irrelavant corrections seem to be your forte.
It is irrelevant that you are calling something that is not a gene a gene? OK.

It depends on the mutation

Indeed. So why do you think mutations could not have increased human brain volume? Functionally, the human and chimp brains, and thus a hypothetical ancestor's, are quite similar.
 
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Loudmouth

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not realy. you believe that those ervs are the result of viral insertions.

We conclude that those insertions are the product of viral insertions because we can directly observe retroviruses producing ERVs in the lab. It isn't a belief.

you belive that the fixation of such insertion (if it's indeed a viral insertion) is almost a random event and so on. so yes- it's a belief.

False. We can directly observe that retroviral insertions are sufficiently random so that they will only rarely (1 in every 50,000 or so insertions) produce the same insertion in two independent events. This is not a belief. This is a conclusion drawn from observations.

do you agree that chimp is different from human by about millions of deletions and insertions? if so any erv isnt in identical position in the genome.

for instance:

abcdefg
compare with:
abccabcdefg

is the letter g in identical position?

The letter g is in an orthologous position. Again, these are ORTHOLOGOUS insertions.
 
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mark kennedy

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It is irrelevant that you are calling something that is not a gene a gene? OK.

It is irrelevant to pick nits over semantics. It appears to be all you do, you certainly have no interest in research or resource material.

Indeed. So why do you think mutations could not have increased human brain volume?

Deleterious effects.
Functionally, the human and chimp brains, and thus a hypothetical ancestor's, are quite similar.

Oh but they are not, that's the whole point. And when it comes to mutations in highly conserved brain related genes especially with regards to mutations, it a dead end.
 
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Loudmouth

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Brain related genes aren't highly conserved; I feel like we have had this discussion before.

There are sequence differences between some brain related genes shared by chimps and humans. You claim that these differences will always produce deleterious effects, yet these differences are not causing deleterious effects. You are simply wrong when you say that any change to these genes will be deleterious.
 
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Loudmouth

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The change of alleles happen a lot of different ways, the CRISPR gene no one has the slightest interest in is one way bacteria adapted the immune system.

There is no interest in CRISPR as it relates to eukaryotic evolution because eukaryotes do not have CRISPR systems.
 
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PsychoSarah

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There is no interest in CRISPR as it relates to eukaryotic evolution because eukaryotes do not have CRISPR systems.
Indeed, I looked up how CRISPR is identifiable in bacteria, and, if I am recalling this correctly, the sequence is a palindrome. It would be very easy to spot if present in eukaryotes.
 
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xianghua

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We conclude that those insertions are the product of viral insertions because we can directly observe retroviruses producing ERVs in the lab. It isn't a belief.

true. but we also know that a retrovirus can be "infected" by the host too. so you cant know if those ervs in the genome are the product of viral insertions, or that retroviruses are the product of host genes.


False. We can directly observe that retroviral insertions are sufficiently random so that they will only rarely (1 in every 50,000 or so insertions) produce the same insertion in two independent events. This is not a belief. This is a conclusion drawn from observations.

not realy. we also need to include fixation and not just insertions. since all ervs in the genomes need to be fixed in the population. so it's not a random event as you may think.


The letter g is in an orthologous position. Again, these are ORTHOLOGOUS insertions.

but it isnt in the same place. by this criteria even if it will be milion base away you can still claim for orthologous position.
 
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tas8831

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tas8831

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It is irrelevant to pick nits over semantics. It appears to be all you do, you certainly have no interest in research or resource material.

It makes a difference when a reporter (you, in this case) makes such errors. It matters because if you repeatedly make errors on the trivial, simple stuff, why should we have confidence that your reporting on highly technical material is any better?
So why do you think mutations could not have increased human brain volume?
Deleterious effects.
Deleterious effects of increased brain volume? Obviously, the mutations we have that are associated with increased brain volume were not deleterious, so your answer makes 0 sense.
Functionally, the human and chimp brains, and thus a hypothetical ancestor's, are quite similar.

Oh but they are not, that's the whole point.

Then your point is simply wrong.

Anatomically, very similar - see these images.

Functionally, chimps have a Broca's area, a Wernicke's area, etc.

Obviously, there are differences (if there were not, they would be identical), but your blanket, unsupported assertion has no merit.

And when it comes to mutations in highly conserved brain related genes especially with regards to mutations, it a dead end.

Mutations in regards to mutations.... Half the time I have no idea what you are trying to claim.
 
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Loudmouth

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true. but we also know that a retrovirus can be "infected" by the host too. so you cant know if those ervs in the genome are the product of viral insertions, or that retroviruses are the product of host genes.

The creation of new viral particles from inserted retroviral genomes is part of the viral life cycle, so I don't see what this has to do with anything.

not realy. we also need to include fixation and not just insertions. since all ervs in the genomes need to be fixed in the population. so it's not a random event as you may think.

Why does fixation make the insertions themselves non-random? Also, there are human ERVs that haven't reached fixation, so fixation isn't a requirement.

but it isnt in the same place.

Yes, it is. The insertion occurs at the same orthologous base. An indel upstream of the insertion site does not change this fact.
 
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xianghua

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The creation of new viral particles from inserted retroviral genomes is part of the viral life cycle, so I don't see what this has to do with anything.
if it's possible that a retrovirus parts can evolve from the host parts- then you cnat know if ervs evolved from retroviruses or the opposite.

Why does fixation make the insertions themselves non-random?

because fixation event can be very non-random. if for instance the retrovirus will insert his parts in a middle of a functional gene- there is a big chance that it will be harmful.


Yes, it is. The insertion occurs at the same orthologous base. An indel upstream of the insertion site does not change this fact.

so i can say the same for the shared ervs between chimp and gorila but not in orangutan and human. can you prove that they are indeed non- orthologous? also: what is the chance that we will find about 6 ervs that are in a similar spots in the genome (about 150000 bases upstream)?
 
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Loudmouth

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if it's possible that a retrovirus parts can evolve from the host parts- then you cnat know if ervs evolved from retroviruses or the opposite.

We know that ERVs are created by retroviruses inserting themselves into the host genome because we can watch that very thing happen in the wild and in the lab.

because fixation event can be very non-random.

The ERV evidence is based on their location in the genome, not the rate at which they are fixed.

if for instance the retrovirus will insert his parts in a middle of a functional gene- there is a big chance that it will be harmful.

Functional DNA makes up around 10% of the human genome. Plenty of regions for retroviruses to insert into.

so i can say the same for the shared ervs between chimp and gorila but not in orangutan and human. can you prove that they are indeed non- orthologous?

You already cited a paper where they stated quite clearly that they couldn't find a single example of an orthologous PtERV shared by gorillas and chimps. What more do you need?

Again, an indel upstream or downstream of an ERV does not change the base that it is actually at. It isn't that hard of a concept to understand. Let's say you have this arrangement:

---GeneA-----GeneB----GeneC
---GeneA--indel---GeneB---GeneC

All of those genes are still orthologous, even though there is an indel. Over 200,000 ERVs are found at the same orthologous base in the chimp and human genomes, and that is smoking gun evidence for common ancestry.

also: what is the chance that we will find about 6 ervs that are in a similar spots in the genome (about 150000 bases upstream)?

Orthologous does not mean "within 150,000 bases".
 
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xianghua

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We know that ERVs are created by retroviruses inserting themselves into the host genome because we can watch that very thing happen in the wild and in the lab.

again: we know that the opposite is possible too.


Functional DNA makes up around 10% of the human genome. Plenty of regions for retroviruses to insert into.

only a belief.


Orthologous does not mean "within 150,000 bases".

if the number of indels doesnt matter then they can be 150,000 away and still be consider as orhtologous.
 
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