PHYL acts to down-regulate TTK88, a transcriptional repressor of neuronal cell fates, by a SINA-dependent mechanism

被引:197
作者
Tang, AH [1 ]
Neufeld, TP [1 ]
Kwan, E [1 ]
Rubin, GM [1 ]
机构
[1] UNIV CALIF BERKELEY,HOWARD HUGHES MED INST,DEPT MOL & CELL BIOL,BERKELEY,CA 94720
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S0092-8674(00)80506-1
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
We show that Tramtrack (TTK88) expression represses neuronal fate determination in the developing Drosophila eye. Phyllopod (PHYL) acts to antagonize this repression by a mechanism that requires Seven In Absentia (SINA) and is associated with decreased TTK88 protein levels, but not reduced ttk88 gene transcription or mRNA stability. We present evidence that SINA, PHYL, and TTK88 physically interact and that SINA interacts genetically and physically with UBCD1, a component of the ubiquitin-dependent protein degradation pathway. Our results suggest a model in which activation of the Sevenless receptor tyrosine kinase induces PHYL expression, which then acts with SINA to target the transcriptional repressor TTK88 for degradation, thereby promoting R7 cell fate specification.
引用
收藏
页码:459 / 467
页数:9
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