I never said you did.
What I said was that your claim that random mutations can't produce de novo genes was a lie.
Well you sure resorted to the ad hominem fallacy quickly. Often they will refer to coopting proceses as mutations but any more they simply refer to it as variation. A de novo gene is exceedingly rare and mistaking one for a mutation is ridiculous.
I then supported this with multiple studies that provide evidence for mutations producing de novo genes.
Thats not what I seen in the source material, in fact they refer to changes of a single base pair as SNV, or a single mucleotied variat. Avout half the human genome is transposable, brain related genes dont fall in that catagory. Vaiations in such highly conserved genes are invariably deleterious. You get cancer, tunors, Parkinsons muliple Sclerosis and a long list of disease and disorders.
Here's an excerpt from the Schlotterer paper:
"Interestingly, a considerable fraction of these RNAs are also associated with ribosomes, suggesting they are actively translated. Such short peptides form proto genes, which can be subject to selection. Through the acquisition of new mutations, proto genes can grow and result in functional de novo genes"
This is a short RNA stran, its been knownnfor some time RNA sequences can be taken from just about anywhere is the genome. When your talking about brain related genes your talking orders of magnitue greater complexity, especially is they are protien coding. You want to compare that to a short, mildly trasposabke RNA strand.
I don't think it can be made much clearer....
Except that's not what studies argued. Transactional co-option in genes is not just 'simple repeats'. The Besenbacher paper highlights that there are insertions/deletions, transitions, transversions and tandem mutations all in de novo gene production in humans.
So far you havnt shown me a singke human de novo gene. Whats more many of these transpositions are somatic, their not going to be inheritable.
This, along with your line from earlier in the thread - that "The hominid line starts 2 mya without precursors and requires at least 60 de novo genes" - is completely unsupported.
Except that what it says in the abstract and described throughout.
To support that, here's that
Wu et al 2011 paper you're so fond of misconstruing:
Our finding of 60 de novo genes, 59 of which are fixed in the human population, suggests that the de novo origin of protein coding genes on the human lineage is not a rare event. Since the chimpanzees and humans shared a common ancestor ∼5–6 million years ago, this indicates that the rate of origin of de novo genes is ∼9.83–11.8 genes per million years, an estimate that is much higher than previously reported.
Where does that 2mya figure come from, by the way?
Paleontology, the fossles average between 400cc and 500cc untill 2 mya. Around that time Homo erectus arives on the scene with nearly human proportions. Thats wrre I get the 2 mya figure.
Even some of the papers the Wu study references (
in this case Knowles and McLysaght A, 2009) indicate there are genetic precursors to de novo genes:
This is the first evidence for entirely novel human-specific protein-coding genes originating from ancestrally noncoding sequences. We estimate that 0.075% of human genes may have originated through this mechanism leading to a total expectation of 18 such cases in a genome of 24,000 protein-coding genes.
Thats .075% for a reason, its exceedingly rare.
To support my case further, here's yet another paper - on de novo genes nonetheless - showing that there ARE precursors present in hominidae de novo gens prior to fixation.
De Novo Genes Arise at a Slow but Steady Rate along the Primate Lineage and Have Been Subject to Incomplete Lineage Sorting
Here, we describe a rigorous search for cases of de novo gene origination in the great apes. We analyzed annotated proteomes as well as full genomic DNA and transcriptional and translational evidence. It is notable that results vary between database updates due to the fluctuating annotation of these genes. Nonetheless we identified 35 de novo genes: 16 human-specific; 5 human and chimpanzee specific; and 14 that originated prior to the divergence of human, chimpanzee, and gorilla and are found in all three genomes. The taxonomically restricted distribution of these genes cannot be explained by loss in other lineages. Each gene is supported by an open reading frame-creating mutation that occurred within the primate lineage, and which is not polymorphic in any species. Similarly to previous studies we find that the de novo genes identified are short and frequently located near pre-existing genes. Also, they may be associated with Alu elements and prior transcription and RNA-splicing at the locus. Additionally, we report the first case of apparent independent lineage sorting of a de novo gene. The gene is present in human and gorilla, whereas chimpanzee has the ancestral noncoding sequence. This indicates a long period of polymorphism prior to fixation and thus supports a model where de novo genes may, at least initially, have a neutral effect on fitness..
It's like I say "Look, water" and you reply "Where?", all while standing knee deep in a puddle.
No and I've had this discussion repeatedly. The last time the key factor were transcritones. Ok, they find a disfuntional protien coding gene in chinpazee and a functional one in humans. All this tell ne is that chimpazees have a similar gene with a broken reading frame.
You know this is all anecdotal and speculative. Darwinians have always argued nutations plus selection but never really prove it except in rare isolated instances. When you equivocte any variation, especially an RNA sequence that has no chance of being inheritable, you grasping at straws
