Yea not surprising at all except there is no cause, just an assumed effect.
-_- the cause is mutations in genes. While the current understanding of genes related to intelligence is not particularly expansive, it's not as if we know of NONE related to it.
In one of the areas of the human genome that would have had to change the most, Human Accelerated Region (HAR), we find a gene that has changed the least over just under 400 million years HAR1F.
-_- that's just straight up incorrect. The HAR regions are named such BECAUSE they change so much, and if you bothered to look up HAR1F, you'd find it is no different in this regard. Not shocking, considering that it wouldn't be labeled as an HAR if it had been highly conserved. Many of the HARs are related to neurodevelopment, did you do no research? Even mentioning them weakens every aspect of your argument, since they demonstrate that many of the genes related to human brain development are highly prone to mutation.
HAR1A even has a secondary structure unique to humans, though chimpanzees have one very similar to it. You unintentionally pointed out one of the main mutations that could have contributed to human intelligence. Nice job, I couldn't have done it better myself. I'm just going to cut out the rest of your post that tries to argue that this brain region is highly conserved and not prone to mutation, because that is factually incorrect.
Perhaps your issue was with the fact that genes in this region are highly conserved in non-human vertebrates. I see no issue, are you assuming that it is present on a chromosome of equal length and at the same location with every vertebrate species? Genes have variable mutation rates within a species, as well as between different species. Conserved doesn't mean exactly the same in every vertebrate species, though. Rather, vertebrates generally have genes analogous to this which mutate relatively infrequently. Yet, in humans, this is a gene which mutates quite frequently. Could be a result of a gene related to preventing mutations being broken in humans while it is functional in most vertebrates. Could explain our high mutation rate overall.
The most dramatic of these ‘human accelerated regions’, HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal– Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal–Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. (An RNA gene expressed during cortical development evolved rapidly in humans, Nature 16 August 2006)
At least you got its function right. Yet, a highly variable gene sequence in our species.
This all has to occur after the chimpanzee human split, while our ancestors were contemporaries in equatorial Africa, with none of the selective pressures effecting our ancestral cousins.[/QUOTE]
-_- that latter half would only be true if this was the sole gene responsible for human intelligence, and it demonstrably is not. You are right in that the form of the gene present in humans is not present in chimps, so it must have appeared in the evolutionary timeline after the evolutionary lines of human and chimp had already split. If you can find any articles on whether or not it is present in Neanderthals, I would be very interested.
This is in addition to no less then 60 de novo (brand new) brain related genes with no known molecular mechanism to produce them.
-_- mutation. Genes can be produced via mutation. I suppose you don't realize that chimps have many analogous genes that are slightly different, so there is no reason that mutations on genes which already existed couldn't be responsible for human intelligence. But hey, let's assume your incorrect assertion has merit and that 60 entirely new genes had to appear in the human evolutionary line after the split between human and chimp evolutionary lines. That gives about 12 million years for mutations to produce these genes, and mutations can be as small as 1 base pair change and as large as the duplication of entire chromosomes. So, I'll be generous and assume all mutations are just 1 base pair. I'll also be generous and assume that the population of organisms ancestral to modern humans had an average of 10,000 individuals born every year, and each individual born had only 10 mutations (compared to what we observe in humans; 40-60). That would mean that after human and chimp evolutionary lines had split, 1200000000000 mutations the size of single base pairs had occurred. Now, I will be generous and assume only 1% of those mutations are additions, and account for the fact that genes are generally around 27,000 base pairs long in humans. That would mean that, within this time period, about 444,444 new genes could be produced just through addition mutations alone. Even if only 1% of these mutations impacted genes at all, that would result in 4444 genes altered. And this is a worst case scenario that doesn't even represent the much more favorable reality. About 9% of the genome is genes, with 8% being regulatory genes and 1% producing proteins with non-regulatory functions. And you are going to throw a fit over a measly 60 genes?
Selection can explain the survival of the fittest but the arrival of the fittest requires a cause:
Which is mutation. Mutations that cause catastrophic failure result in miscarriages or death in early childhood, so those just weed themselves out regardless of the environment.
The de novo origin of a new protein-coding gene from non-coding DNA is considered to be a very rare occurrence in genomes. Here we identify 60 new protein-coding genes that originated de novo on the human lineage since divergence from the chimpanzee. The functionality of these genes is supported by both transcriptional and proteomic evidence. RNA– seq data indicate that these genes have their highest expression levels in the cerebral cortex and testes, which might suggest that these genes contribute to phenotypic traits that are unique to humans, such as improved cognitive ability. Our results are inconsistent with the traditional view that the de novo origin of new genes is very rare, thus there should be greater appreciation of the importance of the de novo origination of genes…(De Novo Origin of Human Protein-Coding Genes PLoS 2011)
Your own source suggests that genes which arise "de novo" are more common than traditionally thought. In no way does it support your position that there is NO mechanism by which these genes arose. It's mutation.
Whatever you think happened one thing is for sure, random mutations are the worst explanation possible. They cannot produce de novo genes and invariably disrupt functional genes.
Demonstrably wrong, as in bacteria, de novo genes are the reason why some can digest nylon now. Beneficial mutations make up about 5% of mutations, with neutral mutations making up a majority and malignant mutations being about 30%. Of course, the worst of that 30% results in organisms that will die before they are able to reproduce, so they are weeded out of the population quite quickly.
Brain related genes do not respond well to changes.
Clearly wrong, since most HARs, the regions of the human genome most prone to change, are related to neurodevelopment.
Two dramatic giant leaps that would have had to occur in order of the human brain to have emerged from ape like ancestors SRGAP2, HAR1F. In addition genes involved with the development of language (FOXP2), changes in the musculature of the jaw (MYH16) , and limb and digit specializations (HACNS1).
The ancestral SRGAP2 protein sequence is highly constrained based on our analysis of 10 mammalian lineages. We find only a single amino-acid change between human and mouse and no changes among nonhuman primates within the first nine exons of the SRGAP2 orthologs. This is in stark contrast to the duplicate copies, which diverged from ancestral SRGAP2A less than 4 mya, but have accumulated as many as seven amino-acid replacements compared to one synonymous change. (Human-specific evolution of novel SRGAP2 genes by incomplete segmental duplication Cell May 2012)
What is the problem with 7 amino acid replacements in a highly conserved brain related gene? The only observed effects of changes in this gene in humans is disease and disorder:
-_- the only effects that would overtly stand out and give reason to check a person's genes would be ones that cause disorder. Do you think we pull aside geniuses to have their genomes sequenced just for their intelligence? Because we don't do that. The vast majority of people that have their genomes sequenced are going to be sick, one way or another.
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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…
Where's the supposed disorder associated with this one?
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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…
Where's the genetic mutation for this one?
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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)
Ok, we have a mutation and a disorder. Fabulous. So, how does this demonstrate that all mutations related to genes that deal with the brain are negative, or, at a minimum, none are beneficial? Because there are very few genes so highly conserved in humans that everyone has them the same (mostly HOX genes). We all have variations in genes related to brain development and function. So, what's the "original, ideal gene"?
The search for variation with regard to this vital gene yielded no beneficial effect upon which selection could have acted.
The only conceivable way the changes happen is relaxed functional constraint which, unless it emerged from the initial mutation perfectly functional it surly would have killed the host.
Why? Incomplete genes are generally broken and don't do anything at all, and their presence allows for a later mutation to hit them and jump start functionality. Heck, humans are full of genes that, if left active, would do survivable amounts of harm. Hence why the majority of genes are regulatory and many exist just to keep other genes from ever being active.
Mutations are found in children with 'developmental delay and brain malformations, including West Syndrome, agenesis of the corpus callosum, and epileptic encephalopathies'.
They are also found in normal, healthy people. There's just no reason to dedicate huge amounts of money to variations in the human genome that result in minimal differences. Since there are so many genes which contribute to our intelligence, notable variations in intelligence are due to combinations of different alleles, not just 1. Hence why humans have brain size ranges, brain structure ranges, etc.
Lucy had a chimpanzee size brain, as did the Taung child, in fact she was kind of smaller then average.
Oh, a child head contained a smaller than average brain? Shocker. Brain size ranges for children are much wider than for adults, due to hormonal cues that impact brain growth happening later in some children than others. Furthermore, you missed the point I made entirely, or that the upper level of Lucy's species, 550 cc, EXCEEDS that of the upper end of the chimp range (500 cc). This means that at least 1 of Lucy's species had a brain demonstrably bigger than chimps. But again, it was never her brain that made her a transitional.
Speaking of transitionals I noticed you don't have much of a taste for Paranthropos right where you would expect a hominid fossil, a period covering a million years and it's just an ape transitional.
420-520 cc for that species. They are distant cousins to the evolutionary line relevant to humans, so there was no reason to bring them up. They aren't considered transitional to humans at all.
Curious, very curious indeed, especially considering our primate cousins are virtually unrepresented in the fossil record.
They didn't live in as good of places for producing fossils as human ancestors did, but they do exist.
https://www.outlookindia.com/public/uploads/articles/2017/4/27/5_630_630.jpg
https://wolvesonceroamed.files.wordpress.com/2013/03/sivapithecus.jpg
These also don't get as much press as human transitionals, since we're kinda a self-centered species.
Ok I'm not buying that scientists know as much about the weather 800,000 years ago. I'm really not going to buy the proposition that you can just insert natural selection every time you are missing an actual molecular cause.
It's not missing, it's mutation. I've run out of time, however, and will have to address the rest of your post later.
