Simske J S, Kaech S M, Harp S A, Kim S K
Department of Developmental Biology, Stanford University Medical School, California 94305-5427, USA.
Cell. 1996 Apr 19;85(2):195-204. doi: 10.1016/s0092-8674(00)81096-x.
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.
在秀丽隐杆线虫中，锚定细胞信号通过激活保守的受体酪氨酸激酶途径诱导Pn.p细胞形成外阴。lin-2和lin-7突变体表现出与该信号通路有缺陷时所观察到的表型相似的无外阴表型。我们发现LIN-7是一种与细胞连接相关的蛋白质，它与LET-23受体酪氨酸激酶结合。LET-23也定位于细胞连接，并且LIN-2和LIN-7都是这种定位所必需的。LET-23的过表达挽救了lin-2或lin-7的无外阴表型，这表明受体密度增加可以补偿定位错误。这些结果表明，LET-23受体正确定位于Pn.p细胞连接对于信号传导活性是必需的。
