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Access through your institution Buy or subscribe In their studies, the authors concentrated on the ectopic bristles seen in the eyes of flies in which Hsp90 function had been reduced through
mutation or pharmacological inhibition. Offspring from flies fed an Hsp90-inhibiting drug were bred and selected for the eye bristle phenotype, for 13 generations, in the absence of the
drug. The penetrance of the phenotype increased in response to selection and remained even when Hsp90 function was restored. However, as the strain of flies used in the experiment was nearly
isogenic, genetic variation was unlikely to account for the fixation of the ectopic eye-bristle phenotype, as was previously thought. Instead, it was more likely that epigenetic changes
affecting chromatin structure had occurred. In support of this idea, when flies from the F6 generation were treated with a histone deacetylase inhibitor — resulting in an increase in histone
acetylation — the percentage of individuals showing ectopic eye bristles decreased significantly. The authors also identified a further link between chromatin structure and ectopic eye
bristles. A similar bristle phenotype to that seen in flies with compromised Hsp90 function was found in mutants of nine different _trithorax_ group (_trx_) genes, which exhibit
hypoacetylation. Once again, the phenotype was reduced by histone deacetylase inhibitor treatment. Selection studies on the most severe _trx_ mutant showed that, although the mutation is
required initially in the mother to generate the ectopic eye bristles, after selection it is not required to maintain the phenotype. It seems, therefore, that _trx_ mutations induce ectopic
outgrowths by altering chromatin structure in the egg and then an unknown epigenetic mechanism results in their fixation. This indicates that Hsp90 removal might induce epigenetic changes,
possibly through an interaction with Trx proteins. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this
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support REFERENCES ORIGINAL RESEARCH PAPER * Sollars, V. et al. Evidence for an epigenetic mechanism by which Hsp90 acts as a capacitor for morphological evolution. _Nature Genet._ 33, 70–74
(2003) Article CAS Google Scholar FURTHER READING * Rutherford, S. L. et al. Hsp90 as a capacitor for morphological evolution. _Nature_ 396, 336–342 (1998) Article CAS Google Scholar
* Queitsch, C. et al. Hsp90 as a capacitor of phenotypic variation. _Nature_ 417, 618–624 (2002) Article CAS Google Scholar * Rutherford, S. L. & Henikoff, S. Quantitative
epigenetics. _Nature Genet._ 33, 6–8 (2003) Article CAS Google Scholar Download references Authors * Catherine Baxter View author publications You can also search for this author inPubMed
Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Baxter, C. Now you see it ... now you don't!. _Nat Rev Genet_ 4, 81 (2003).
https://doi.org/10.1038/nrg1006 Download citation * Issue Date: 01 February 2003 * DOI: https://doi.org/10.1038/nrg1006 SHARE THIS ARTICLE Anyone you share the following link with will be
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