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Heterosis and gene duplicati

Marc GIRONDOT p75783 mgi at ccr.jussieu.fr
Thu Feb 11 04:05:06 EST 1993

In article <1lcc8uINNq71 at uniwa.uwa.edu.au> andrewh at uniwa.uwa.edu.au (Andrew Hobbs) writes:
>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.au
Marc Girondot
Laboratoire de Biochimie du Developpement, Paris

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