LET-23 receptor localization by the cell junction protein LIN-7 during C-elegans vulval induction

被引:229
作者
Simske, JS
Kaech, SM
Harp, SA
Kim, SK
机构
[1] Department of Developmental Biology, Stanford University Medical School, Stanford
关键词
D O I
10.1016/S0092-8674(00)81096-X
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
In C. elegans, the anchor cell signal induces Pn.p cells to form the vulva by activating a conserved receptor tyrosine kinase pathway. lin-2 and lin-7 mutants exhibit a vulvaless phenotype similar to the phenotype observed when this signaling pathway is defective. We have found that LIN-7 is a cell junction-associated protein that binds to the LET-23 receptor tyrosine kinase. LET-23 is also localized to the cell junctions, and both LIN-2 and LIN-7 are required for this localization. LET-23 overexpression rescues the lin-2 or lin-7 vulvaless phenotype, suggesting that increased receptor density can compensate for mislocalization. These results suggest that proper localization of LET-23 receptor to the Pn.p cell junctions is required for signaling activity.
引用
收藏
页码:195 / 204
页数:10
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