Journal
NATURE GENETICS
Volume 33, Issue 1, Pages 70-74Publisher
NATURE AMERICA INC
DOI: 10.1038/ng1067
Keywords
-
Categories
Funding
- NCI NIH HHS [R01 CA105349] Funding Source: Medline
- NIAAA NIH HHS [R01 AA012276] Funding Source: Medline
Ask authors/readers for more resources
Morphological alterations have been shown to occur in Drosophila melanogaster when function of Hsp90 (heat shock 90-kDa protein 1alpha, encoded by Hsp83) is compromised during development(1). Genetic selection maintains the altered phenotypes in subsequent generations(1). Recent experiments have shown, however, that phenotypic variation still occurs in nearly isogenic recombinant inbred strains of Arabidopsis thaliana(2). Using a sensitized isogenic D. melanogaster strain, iso-Krlf-1, we confirm this finding and present evidence supporting an epigenetic mechanism for Hsp90's capacitor function, whereby reduced activity of Hsp90 induces a heritably altered chromatin state. The altered chromatin state is evidenced by ectopic expression of the morphogen wingless in eye imaginal discs and a corresponding abnormal eye phenotype, both of which are epigenetically heritable in subsequent generations, even when function of Hsp90 is restored. Mutations in nine different genes of the trithorax group that encode chromatin-remodeling proteins also induce the abnormal phenotype. These findings suggest that Hsp90 acts as a capacitor for morphological evolution through epigenetic and genetic mechanisms.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available