Evidence for an epigenetic mechanism by which Hsp90 acts as a capacitor for morphological evolution
Evidence for an epigenetic mechanism by which Hsp90 acts as a capacitor for morphological evolution
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DOI：
10.1038/ng1067
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发表时间：
2003-01-01
期刊：
影响因子：
30.8
通讯作者：
Ruden, DM
中科院分区：
文献类型：
--
作者：
Sollars, V;Lu, XY;Ruden, DM
当Hsp 90（热休克90-kDa蛋白1 α，由Hsp 83编码）的功能在发育过程中受损时，黑腹果蝇的形态学改变已被证明发生（1）。遗传选择在后代中保持改变的表型（1）。然而，最近的实验表明，表型变异仍然发生在拟南芥的近等基因重组近交系中（2）。使用致敏的等基因D.黑腹果蝇品系iso-Krlf-1，我们证实了这一发现，并提出了支持Hsp 90电容器功能的表观遗传机制的证据，从而降低Hsp 90的活性诱导遗传改变的染色质状态。改变的染色质状态证明异位表达的形态发生无翅在眼睛的成虫盘和相应的异常的眼睛表型，这两者都是表观遗传遗传在后代中，即使当Hsp 90的功能恢复。编码染色质重塑蛋白的三胸组的9个不同基因的突变也诱导异常表型。这些发现表明，热休克蛋白90作为一个电容器的形态进化通过表观遗传和遗传机制。
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.