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SMRTER, a Drosophila nuclear receptor coregulator, reveals that EcR-mediated repression is critical for development
被引:170
作者:
Tsai, CC
Kao, HY
Yao, TP
McKeown, M
Evans, RM
机构:
[1] Salk Inst Biol Studies, Howard Hughes Med Inst, Gene Express Lab, La Jolla, CA 92037 USA
[2] Salk Inst Biol Studies, Mol Biol & Virol Lab, La Jolla, CA 92037 USA
关键词:
D O I:
10.1016/S1097-2765(00)80365-2
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
The Drosophila ecdysone receptor (EcR)/ultraspiracle (USP) heterodimer is a key regulator in molting and metamorphoric processes, activating and repressing transcription in a sequence-specific manner. Here, we report the isolation of an EcR-interacting protein, SMRTER, which is structurally divergent but functionally similar to the vertebrate nuclear corepressors SMRT and N-CoR. SMRTER mediates repression by interacting with Sin3A, a repressor known to form a complex with the histone deacetylase Rpd3/HDAC. Importantly, we identify an EcR mutant allele that fails to bind SMRTER and is characterized by developmental defects and lethality. Together, these results reveal a novel nuclear receptor cofactor that exhibits evolutionary conservation in the mechanism to achieve repression and demonstrate the essential role of repression in hormone signaling.
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页码:175 / 186
页数:12
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