The C-elegans E2F-and DP-related proteins are required for embryonic asymmetry and negatively regulate Ras/MAPK signaling

被引:85
作者
Page, BD
Guedes, S
Waring, D
Priess, JR
机构
[1] Fred Hutchinson Canc Res Ctr, Div Basic Sci, Seattle, WA 98109 USA
[2] Univ Washington, Dept Zool, Seattle, WA 98195 USA
[3] Univ Washington, Mol & Cellular Biol Program, Seattle, WA 98195 USA
[4] Howard Hughes Med Inst, Seattle, WA 98109 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1016/S1097-2765(01)00193-9
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
Early C. elegans embryos exhibit protein asymmetries that allow rapid diversification of cells. Establishing these asymmetries requires the novel protein MEX-5. We show that mutations in the efl-1 and dpl-1 genes cause defects in protein localization resembling defects caused by mutations in mex-5. efl-1 and dpl-1 encode homologs of vertebrate E2F and DP proteins that regulate transcription as a heterodimer. efl-l and dpl-1 mutants have elevated levels of activated Map kinase in oocytes. Their mutant phenotype and that of mex-5 mutants can be suppressed by reducing Ras/Map kinase signaling. We propose this signaling pathway has a role in embryonic asymmetry and that EFL-1/DPL-1 control the level of Map kinase activation.
引用
收藏
页码:451 / 460
页数:10
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