I am hoping to get some discussion on heterosis and gene duplication.
Somewhere I have read that if you get a single gene heterosis effect
then one would expect to observe gene duplication so that very rapidly
all individuals in the population would enjoy the advantage previously
available to the heterozygotes. Is this so? (It seems obvious to me if
gene duplication events are relatively common).
If the above is true, why hasn't gene duplication been observed with
the normal and mutated globin genes with regard to sickle cell anemia in
malarial areas? Gene duplication has obviously occurred as shown by the
number of globin pseudo-genes.
Does the lack of such a functional change indicate the low rate of gene
duplication (and hence just hasn't happended yet), could it indicate the
difficulties of recombination between chromosomes differing due to
tandem duplication of DNA, or am I missing something?
If this has already been discussed elsewhere then could someone direct
me in the right direction.
Dept of Biochemistry
University of Western Australia
andrewh at uniwa.uwa.edu.au