Well we've had a few examples of gene names eg APOL1, APOL4, CARD18
This new one C4C1001 does not follow that convention ie four letters and a number but then I have no idea how they choose the names and thats why I said I was intrigued. Do you have any ideas about how they name genes?
Again, no one is writing papers on whether chimps have genes that humans do not.
You originally stated that chimps and humans both have genes that the other does not have. Please provide evidence for your claims or alternatively retract your remark.
But you vastly underestimate the importance of the olfactory genes. While the smell sensors are small and not physically visible they evidently are of critical importance for tetrapods because of the amount of genetic and brain real estate dedicated to them.
You also stated that while humans and chimps share 98% of their genome it was the genes that were different. The article referring to the olfactory genes refers to large numbers of pseudo genes differing between the two species. Infact pseudogenes outnumber real genes by a significant order of magnitude in this article. This suggests that it's not so much the genes but the non functional parts of the DNA that are most different between the two species.
Your reference/evidence therefore contradicts your own argument.
You have had a number of examples presented to you from a variety of papers.
Disagree. You have named only one potential candidate ie C4C1001 which non of us have been able to cross reference with any other source. We still haven't even established if this a real gene or not. Even if you were to tell me that it were, you don't have any cross reference to cement your claim. We can't continue with this debate while Percy continues to make wild claims with no substance behind them.
Still lets give you yet another example to see how you fudge and slide your way around it
There is no obligation upon me to explain what I intend to use this information for as Percy would have you believe.
Ahh finally we have something to work with ie MYH16. It's not a case of trying to wriggle out of anything. If you make a claim like the one Percy made you should be able to back it up with evidence. I note that the evidence had to come from you and not Percy?
but if you'd like to do that then the thread's open and available
Ok in that case I will continue...
I think I have been right all along in pressing for proper identification of a gene difference. The example we have is MHY16 which is quite a good example as it is functional in chimps but not in humans. One of the reasons that it is not functional in humans is due to a frameshift.
MHY16 is classed as a defective frame-shifted allele in humans. Frame-shift is when DNA across species, which may be very similar, (as in the case of humans and chimps) produces very different genes. ie sequences of DNA which are almost identical will produce different proteins because the start and end points for reading the code are different. Maybe WK or one of the other biologists here could elaborate on this point.
One point about frameshift mutations is that their impact is likely to be very significant and more so than one might expect.
If we take a phrase ie
THE CAT ATE THE RAT END where END represents the stop codon and then introduce a frameshift on this we might get something like
THE CAA TAT ETH ERA TEN D
As you can see the meaning of the sentence is completely lost and the full stop has gone too. Any subsequent sentence could also become gibberish. The few examples of frameshift mutations that I have come across in humans often have terrible consequences eg Duchenne muscular dystrophy and Tay Sachs. If you know of any beneficial mutations that would be intriguing.
Do you mean a modern contemporary spontaneous beneficial frameshift mutation in the human population?
Yes, let's focus on humans rather than chimpanzees for the time being. I would be interested in any human to human examples of frameshifted alleles which might generate new traits or features for an individual.
Only from this context can we then move on to presuppose frameshifting across the species.
I looked it up and the actual mutation in the human lineage is a 2 base deletion in exon 18 of the gene. This deletion introduces a stop codon about 30 bases further downstream. This results in the protein being truncated from its expected size of 223 kilodaltons down to 76 kilodaltons.
In this MYH16 mutation, it turns out that this frameshift caused a punctuation mark (aka a stop codon) to just pop up – so the protein is cut off far sooner than it should be! Not too good for any traits relying on that protein.
So far from it actually pushing the stop codon further downstream as we had previously implied it appears that the stop codon appears earlier in the sequence. If you were a software engineer you could think of it as like commented out code.