Bonus, a Drosophila homolog of TIF1 proteins, interacts with nuclear receptors and can inhibit βFTZ-F1-dependent transcription

被引:79
作者
Beckstead, R
Ortiz, JA
Sanchez, C
Prokopenko, SN
Chambon, P
Losson, R
Bellen, HJ
机构
[1] Baylor Coll Med, Dept Mol & Cellular Biol, Houston, TX 77030 USA
[2] Baylor Coll Med, Program Dev Biol, Houston, TX 77030 USA
[3] Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA
[4] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA
[5] Coll France, ULP, CNRS,INSERM, Inst Genet & Biol Mol & Cellulaire, F-67404 Illkirch Graffenstaden, France
关键词
D O I
10.1016/S1097-2765(01)00220-9
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 bonus (bon) gene encodes a homolog of the vertebrate TIF1 transcriptional cofactors. bon is required for male viability, molting, and numerous events in metamorphosis including leg elongation, bristle development, and pigmentation. Most of these processes are associated with genes that have been implicated in the ecdysone pathway, a nuclear hormone receptor pathway required throughout Drosophila development. Bon is associated with sites on the polytene chromosomes and can interact with numerous Drosophila nuclear receptor proteins. Bon binds via an LxxLL motif to the AF-2 activation domain present in the ligand binding domain of beta FTZ-F1 and behaves as a transcriptional inhibitor in vivo.
引用
收藏
页码:753 / 765
页数:13
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