The known mutations which lead to the 'red hair' alleles of MC1R are all loss of function mutations. They produce a receptor protein which is broken, in a sense, and so where the wild type would perform its role of promoting melanin production, the red hair variants don't.
Is that right?
Or, do the major variants of MC1R cause the melanocortin 1 receptor to stimulate the melanocytes into eumelanin production while the minor variants of MC1R block the melanocortin 1 receptor from stimulating eumelanin production causing the melanocytes to make mostly pheomelanin instead?
Do you really consider the minor variants of MC1R to be "broken, in a sense"?
This may seem a semantic quibble, but it does get to the very heart of CRR's misunderstanding of genetics as a whole.
And, no, I do not believe you would call this a "loss" of genetic information.
So, again, no information loss. An information difference. Different proteins resulting from the different nucleotide sequences. Different proteins having different effects upon the system.
And, as often happens with evolution, some of the minor variants convey some advantage in an environment and become the major variants in a population.
CRR is not completely off on this one.
Since he wouldn't know why, I'll disagree.
Edited by AZPaul3, : No reason given.
Edited by AZPaul3, : affect/effect. I still have trouble with this.