Over the last decade, there has been growing evidence (cited by Pigliucci, 2002) that Hsp90, traditionally thought of as a capacitor for environmental change, may be able to canalise genetic change (mutations) as well. Early research in this area investigated the effects of inhibition of Hsp90 on qualitative and discrete quantitative traits in various organisms.
Recently, however, Debat, et. al. have investigated the role of Hsp90 in genetic canalisation of a more complex quantitative trait, wing shape of D. Melanogaster. Hsp90 activity was inhibited in three different experiments; by adding geldanamycin (a known Hsp90 inhibitor) to diets, by the addition of Hsp83 (the gene encoding Hsp90) mutant chromosomes into fly genomes, and by introgression of a specific Hsp83 mutant allele into the fly genome.
Wing shape was measured using the complex methods of “geometric morphometrics”, and their results were very surprising - no increase in phenotypic variation was observed when Hsp90 was inhibited in geldanamycin and mutant chromosome experiments, but an increase was observed in the introgression experiment.
These mixed results led the authors to propose that Hsp90 might not play as central a role in genetic canalisation as initially thought, and may simply be playing a small part in a more complex,as-yet undefined system.
Clearly, the scientific community is at a very young stage in the understanding of the role of Hsp90 in masking genetic variation. Further research can perhaps shed some more light on the issue, and could particularly focuse on the mechanism of genetic canalisation of Hsp90.
References
Pigliucci, M. (2002). Buffer Zone. Nature, vol 417, p598-99)
Debat, V., et.al. (2006) Hsp90 and the quantitative variation of wing shape in D. melanogaster. Evolution, 60 (12): 2529-2538
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