dpl-1 DP and efl-1 E2F act with lin-35 Rb to antagonize Ras signaling in C-elegans vulval development
dpl-1 DP and efl-1 E2F act with lin-35 Rb to antagonize Ras signaling in C-elegans vulval development
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DOI：
10.1016/s1097-2765(01)00194-0
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发表时间：
2001-03-01
期刊：
影响因子：
16
通讯作者：
Horvitz, HR
中科院分区：
文献类型：
--
作者：
Ceol, CJ;Horvitz, HR
合成多外阴(SynMuv)基因定义了两条功能冗余的通路，在秀丽线虫外阴诱导过程中拮抗RTK/RAS信号。SynMuv基因LIN-35编码一种类似于哺乳动物肿瘤抑制基因pRb的蛋白质，并被认为是一种转录抑制因子。使用哺乳动物细胞的研究表明，pRB可以通过抑制DP/E2F介导的转录激活来阻止细胞周期进展。我们鉴定了线虫编码类似于DP或E2F的蛋白的基因。其中两个基因DPL-1 DP和EFL-1 E2F的功能丧失突变导致了与LIN-35RB功能丧失突变相同的外阴异常。我们认为，在外阴发育过程中，DPL-1DP和EFL-L E2F不是被LIN-35RB抑制，而是与LIN-35RB一起发挥转录抑制作用，拮抗RTK/RAS信号。
The synthetic multivulva (synMuv) genes define two functionally redundant pathways that antagonize RTK/Ras signaling during Caenorhabditis elegans vulval induction. The synMuv gene lin-35 encodes a protein similar to the mammalian tumor suppressor pRB and has been proposed to act as a transcriptional repressor. Studies using mammalian cells have shown that pRB can prevent cell cycle progression by inhibiting DP/E2F-mediated transcriptional activation. We identified C. elegans genes that encode proteins similar to DP or E2F. Loss-of-function mutations in two of these genes, dpl-1 DP and efl-1 E2F, caused the same vulval abnormalities as do lin-35 Rb loss-of-function mutations. We propose that rather than being inhibited by lin-35 Rb, dpl-1 DP and efl-l E2F act with lin-35 Rb in transcriptional repression to antagonize RTK/Ras signaling during vulval development.