In article <1lcc8uINNq71 at uniwa.uwa.edu.au> andrewh at uniwa.uwa.edu.au (Andrew Hobbs) writes:
>Hi,
>>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).
It seems a good way to have some advantage... if the duplication is possible.
But it is not always. See for example the RIP system who provoke rapid
mutations on a duplicated sequences on the genome (I think it is on
E coli ? ). Of course some particular sequences are protected (rRAN...).
See also the MIP system (I don't remeber for which organism) who produce
this time a rapid methylation of duplicated sequences who inactivated it.
>>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.
It is well known that duplication of gene in mammalian genome (by transgenese)
leads often a inactivation of the new copyi after 5 or 6 generations...
but is it general ?
>>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.
>>Andrew Hobbs
>Dept of Biochemistry
>University of Western Australia
>>andrewh at uniwa.uwa.edu.auMarc Girondot
Laboratoire de Biochimie du Developpement, Paris
