Is it a hoax?

[AV1611VET]

.

 

[PsychoSarah]

Well, apart from MYH16 allowing for smaller jaw muscles and a larger cranium.
And SRGAP2C causing more dendrites to connect brain neurons making the brain more dense.
And ARHGAP11B causing our neocortex to grow more dense and our brains to develop folds.

I guess apart from these and several other examples the "brain related genes do not respond well to changes".

There's a recent one that's beginning to become more frequent in various populations that results in needing fewer hours of sleep every night. People with this mutation need only 6 hours of sleep to feel rested, and thus far, no negative side effects of this mutation have been identified.

 

[PsychoSarah]

The cranial capacity Sarah, brain related genes do not respond well to changes.

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

If it's unlikely that legs, arms and teeth being so different argues strongly against common ancestry then what about something as conserved as brain related genes.

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.

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.

 

[Loudmouth]

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

That is not what the theory of evolution states, which is the theory you are challenging. You are literally citing mutations as evidence against a theory that predicts the existence of mutations.

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

According to you, there should only be one species on Earth since all other species would have genetic differences compared to this one species which you claim they could not survive.

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

You have already been shown the causes multiple times now.

 

[Loudmouth]

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).

Yes, one of the most abundant out of the 425 ERV insertions they looked at. They only looked at 0.2% of the total ERVs in the chimp genome. You can't make sweeping arguments about all chimp ERVs when you have only looked at 0.2% of them.

They can be found in African great apes but not in humans.

And they are not found at orthologous positions, just as the phylogenetic argument predicts.

 

[Loudmouth]

we actually do. first: i gave at least one example of such a case with the herv-k . secondly: i also gave about 20 potential cases that cant be ignore.

They weren't ignored. They were actually looked at, and the authors were unable to find a single unambiguous orthologous PtERV insertion shared between ape species. Read the paper.

also remember that chimp and human are about 2% different. so even their own orthologous ervs arent realy orthologous but in a similar spots in the genome.

Please back up this claim.

another interesting point is that : "PTERV1 does not share high sequence identity to any known retrovirus". as we can expect if retroviruses evolved from the host and not the opposite.

Why would we expect this?

 

[xianghua]

They weren't ignored. They were actually looked at, and the authors were unable to find a single unambiguous orthologous PtERV insertion shared between ape species.

as i said: they arent sure. so they can be indeed orthologous. they are also in a similar spots on the genome. so their distribution isnt random at all.

Please back up this claim.

it's just a fact that chimp is at least 2% different from human. so even their suppose orthologous ervs arent realy orthologous.

Why would we expect this?

because it's support the possibility the retroviruses evolved from parts of the human genome and not the opposite.

 

[Loudmouth]

as i said: they arent sure. so they can be indeed orthologous.

Let us know when they actually find one. Until then, every confirmed position for a PtERV insertion is found at a non-orthologous position.

they are also in a similar spots on the genome. so their distribution isnt random at all.

They aren't found at similar spots. Being within 200,000 base pairs is not "similar". Also, no one has ever claimed that the distribution of retroviral insertion is completely random. All they have ever claimed is that bias is low enough that it can't explain why 99.9% of human ERVs are found at the same location in the chimp genome.

it's just a fact that chimp is at least 2% different from human. so even their suppose orthologous ervs arent realy orthologous.

Why would being 2% different prevent those ERVs from being at orthologous positions? You still haven't explained that.

because it's support the possibility the retroviruses evolved from parts of the human genome and not the opposite.

How so?

 

[xianghua]

They aren't found at similar spots. Being within 200,000 base pairs is not "similar".

realy? 100,000 bases (and not 200,000 as you said) from about 3 bilion is about less then 1\30000 of the genome. so their positions are almost identical if we look at the entire genome.

Also, no one has ever claimed that the distribution of retroviral insertion is completely random. All they have ever claimed is that bias is low enough that it can't explain why 99.9% of human ERVs are found at the same location in the chimp genome.

i also gave sternberg example of the rat vs mouse insertions. they look almost identical. but they arent the result of shared insertions. so we can get many shared insertions without a common deascent. therefore shared insertions cant be evidence for a common descent.

Why would being 2% different prevent those ERVs from being at orthologous positions? You still haven't explained that.

because the difference? even if you had only one base difference before or after an erv on the genome, then they arent in identical positions compare to the chimp genome. simple.

so or so, the claim about ervs as evidence for a common descent is false.

 

[Loudmouth]

realy? 100,000 bases (and not 200,000 as you said) from about 3 bilion is about less then 1\30000 of the genome. so their positions are almost identical if we look at the entire genome.

BAC clones can vary from 100 to 300 thousand, or even larger. That isn't a similar position in the genome. It certainly isn't orthologous.

i also gave sternberg example of the rat vs mouse insertions. they look almost identical. but they arent the result of shared insertions.

All of them?

How many insertions did they look at, and how many insertions are there in those genomes?

so we can get many shared insertions without a common deascent.

How many is "many"? There are 203,000 ERV insertions in the human genome, and all but ~100 of them are found at an orthologous position in the chimp genome. That can't happen through independent insertions.

because the difference? even if you had only one base difference before or after an erv on the genome, then they arent in identical positions compare to the chimp genome. simple.

BALONEY!!!!! Let's look at an example:


Human: AATATACCGCGGGAGGG---ERV--GGAGTTACCTAAGT
Chimp: AATATACTGCGGGAGGG---ERV--GGAGTTACCTAAGT

Are you telling me that because of that one substitution mutation that those ERVs are not at orthologous positions? Seriously?

so or so, the claim about ervs as evidence for a common descent is false.

You haven't shown that any of it is false.

 

[xianghua]

BAC clones can vary from 100 to 300 thousand, or even larger. That isn't a similar position in the genome. It certainly isn't orthologous.

so where is your limit between orthologous and non- orthologous? 100 bases away? 1000? 10,000?

How many insertions did they look at, and how many insertions are there in those genomes?

according to sternberg article a lots of them:

"Despite the different fates of SINE families, the number of SINEs inserted after speciation in each lineage is remarkably similar: ~300,000 copies…Figure 9c displays the lineage-specific SINE densities on rat chromosome 10 and in the mouse orthologous blocks, showing a stronger correlation than any other feature. The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature, independent of the primary sequence of the SINE and effective over regions smaller than isochores"

https://evolutionnews.org/2010/03/signs_in_the_genome_part_2/

"Are you telling me that because of that one substitution mutation that those ERVs are not at orthologous positions? Seriously?"-

no. i actually refer to insertions and deletions. in those cases any erv isnt a true orthologous.

You haven't shown that any of it is false.

sfs claimed that if i am right then we should find shared insertions in a 2 random species. and we indeed found such cases.

 

[Loudmouth]

so where is your limit between orthologous and non- orthologous? 100 bases away? 1000? 10,000?

Orthologous means the base that was inherited from the common ancestor. That's 1 base.

according to sternberg article a lots of them:

Of those transposon insertions, how many do not produce the predicted phylogeny?

no. i actually refer to insertions and deletions. in those cases any erv isnt a true orthologous.

Orthologous does not mean 100% identity, so I don't see how your criticism matters. Orthology allows for evolution of those sequences since common ancestry. An orthologous gene shared by humans and chimps can differ by 2%, and it is still orthologous.

sfs claimed that if i am right then we should find shared insertions in a 2 random species. and we indeed found such cases.

That is not the case. The distribution of ERVs in species produces the predicted phylogenetic signal. We would absolutely predict that evolutionary mechanisms would produce a few exceptions to the predicted pattern due to incomplete lineage sorting, homoplasies, and low numbers of species in a phylogeny. However, these few exceptions should be swamped by the phylogenetic signal, and they are.

 

[xianghua]

Orthologous means the base that was inherited from the common ancestor. That's 1 base.

im talking about the position on the genome. if the erv is on another chromosom you will still consider it as an orthologous sequence?

Of those transposon insertions, how many do not produce the predicted phylogeny?

as far as i aware about every one of them, because they are different kind of sine sequences.

Orthologous does not mean 100% identity, so I don't see how your criticism matters. Orthology allows for evolution of those sequences since common ancestry. An orthologous gene shared by humans and chimps can differ by 2%, and it is still orthologous.

see above. we are talking about the position on the genome.

That is not the case. The distribution of ERVs in species produces the predicted phylogenetic signal. We would absolutely predict that evolutionary mechanisms would produce a few exceptions to the predicted pattern due to incomplete lineage sorting, homoplasies, and low numbers of species in a phylogeny. However, these few exceptions should be swamped by the phylogenetic signal, and they are.

not realy. first: how many ervs are shared between chimp and human but not gorila? secondly: that was sfs prediction. and i showed that this prediction doesnt hold water. also remember that i gave an example of several shared insertions and even the paper conclude that it was difficult to conclude the correct phylogeny. so the claim about "phylogenetic signal" doesnt hold water too.

 

[Loudmouth]

im talking about the position on the genome. if the erv is on another chromosom you will still consider it as an orthologous sequence?

That would be conditional, since there are two chimp chromosomes (chromosomes 2A and 2B) that are orthologous to a single human chromosome (chromosome 2) due to a chromosomal fusion in the human lineage.

as far as i aware about every one of them, because they are different kind of sine sequences.

References?

not realy. first: how many ervs are shared between chimp and human but not gorila?

I would suspect very few ERVs would be specific to the chimp/human lineage since there was very little time between those divergence times. The chimp and human lineages split 5-7 million years ago, and there are fewer than 100 human specific ERVs out of the 203,000 ERVs found in the human genome.

secondly: that was sfs prediction. and i showed that this prediction doesnt hold water.

You didn't show this. We have shown that you are wrong about this claim.

also remember that i gave an example of several shared insertions and even the paper conclude that it was difficult to conclude the correct phylogeny. so the claim about "phylogenetic signal" doesnt hold water too.

If you find 5 insertions that violate the predicted pattern and 200,000 insertions that produce the predicted pattern then the phylogenetic signal is there. It holds water.

 

[xianghua]

References?

from sternberg article:

https://evolutionnews.org/2010/03/beginning_to_decipher_the_sine/

"We have two genomes that went their separate ways 22 million years ago. We have two lineages that have been subjected to different historical events. Yet, when we compare the chromosome locations of mouse B1s/B2s/B4s with those of rat IDs, they look almost the same. Where the ID SINEs rise in density, so do the B1s/B2s/B4s SINEs; where the ID SINE levels decrease, so also do the B1s/B2s/B4s SINE levels. Independent mutational events have generated equivalent genomic patterns. How can we causally account for this striking pattern?
In the paper written by Francis Collins and his colleagues, under the heading Co-localization of SINEs in rat and mouse1, we read:

“The cause of the unusual distribution patterns of SINEs…is apparently a conserved feature, independent of the primary sequence of the SINE…”"

I would suspect very few ERVs would be specific to the chimp/human lineage since there was very little time between those divergence times.

it's very weird that human have about 100 unique ervs when he shared only about few with chimp since their suppose common descent. so we realy need to belieive that in about few my he get about several shared ervs with chimp, and then after few more my he get about 100 new ervs.

You didn't show this. We have shown that you are wrong about this claim.

simply wrong:

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

If you find 5 insertions that violate the predicted pattern and 200,000 insertions that produce the predicted pattern then the phylogenetic signal is there. It holds water.

but we are talking about phylogenetic tree and not about the amount of shared ervs. so if for instance we found that chimp and gorila shared about several ervs that doesnt exist in human- this case falsified the claim about hierarchical tree. so where is your strong signal in this case?

 

[Loudmouth]

from sternberg article:

https://evolutionnews.org/2010/03/beginning_to_decipher_the_sine/

"We have two genomes that went their separate ways 22 million years ago. We have two lineages that have been subjected to different historical events. Yet, when we compare the chromosome locations of mouse B1s/B2s/B4s with those of rat IDs, they look almost the same. Where the ID SINEs rise in density, so do the B1s/B2s/B4s SINEs; where the ID SINE levels decrease, so also do the B1s/B2s/B4s SINE levels. Independent mutational events have generated equivalent genomic patterns. How can we causally account for this striking pattern?
In the paper written by Francis Collins and his colleagues, under the heading Co-localization of SINEs in rat and mouse1, we read:

“The cause of the unusual distribution patterns of SINEs…is apparently a conserved feature, independent of the primary sequence of the SINE…”"

Almost is not the same as orthologous. You need to show that they are found at orthologous positions, and compare the number of insertions that don't conform to the expected phylogeny with those that do.

it's very weird that human have about 100 unique ervs when he shared only about few with chimp since their suppose common descent. so we realy need to belieive that in about few my he get about several shared ervs with chimp, and then after few more my he get about 100 new ervs.

The common ancestor already had those shared insertions, and those were the results of tens of millions of years of accumulation.

simply wrong:

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

None of those insertions have been shown to be at orthologous positions in the chimp/bonobo and gorilla genomes.

so if for instance we found that chimp and gorila shared about several ervs that doesnt exist in human- this case falsified the claim about hierarchical tree. so where is your strong signal in this case?

To be precise, they need to be ORTHOLOGOUS insertions, not simply the same retrovirus.

 

[xianghua]

Almost is not the same as orthologous.

but even orthologous position isnt identical. so there is no big difference.

None of those insertions have been shown to be at orthologous positions in the chimp/bonobo and gorilla genomes.

again- wrong :

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

"We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome"

 

[Loudmouth]

but even orthologous position isnt identical. so there is no big difference.

It is identical.

again- wrong :

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

"We identified a human endogenous retrovirus K (HERV-K) provirus that is present at the orthologous position in the gorilla and chimpanzee genomes, but not in the human genome"

Yes, we do find a handful of exceptions due to incomplete lineage sorting out of the hundreds of thousands that conform to the expected phylogeney. Again, the evidence is the phylogenetic signal that stands above the noise created by homoplasy and incomplete lineage sorting.

 

[xianghua]

It is identical.

if so human and chimp arent share even one orthologous (because their position on the genome isnt identical).

Yes, we do find a handful of exceptions due to incomplete lineage sorting out of the hundreds of thousands that conform to the expected phylogeney. Again, the evidence is the phylogenetic signal that stands above the noise created by homoplasy and incomplete lineage sorting.

and again- it doesnt prove any common descent. since their insertions and fixations arent random at all. you also cant explain how some creatures survived before they infected by the retrovirus.

 

[Loudmouth]

if so human and chimp arent share even one orthologous (because their position on the genome isnt identical).

Prove it. Also, please include a definition of orthologous. I have tried to educate you on how the word is used, but it has proven to be a worthless cause. Perhaps you can educate yourself.

and again- it doesnt prove any common descent. since their insertions and fixations arent random at all. you also cant explain how some creatures survived before they infected by the retrovirus.

They are random enough that they won't produce the same insertion more than 99% of the time. This is directly observable.