Nilsson L, Li X, Tiensuu T, Auty R, Greenwald I, Tuck S
Umeå Center for Molecular Pathogenesis, Umeå University, S-901 87 Umeå, Sweden.
Development. 1998 Dec;125(23):4809-19. doi: 10.1242/dev.125.23.4809.
Induction of vulval fates in the C. elegans hermaphrodite is mediated by a signal transduction pathway involving Ras and MAP kinase. Previous genetic analysis has suggested that two potential targets of this pathway in the vulva precursor cells are two novel proteins, LIN-25 and SUR-2. In this report, we describe further studies of lin-25. The results of a genetic mosaic analysis together with those of experiments in which lin-25 was expressed under the control of an heterologous promoter suggest that the major focus of lin-25 during vulva induction is the vulva precursor cells themselves. We have generated antisera to LIN-25 and used these to analyse the pattern of protein expression. LIN-25 is present in all six precursor cells prior to and during vulva induction but later becomes restricted to cells of the vulval lineages. Mutations in genes in the Ras/MAP kinase pathway do not affect the pattern of expression but the accumulation of LIN-25 is reduced in the absence of sur-2. Overexpression of LIN-25 does not rescue sur-2 mutant defects suggesting that LIN-25 and SUR-2 may function together. LIN-25 is also expressed in the lateral hypodermis. Overexpression of LIN-25 disrupts lateral hypodermal cell fusion, suggesting that lin-25 may play a role in regulating cell fusions in C. elegans.
秀丽隐杆线虫雌雄同体中阴门命运的诱导是由一条涉及Ras和丝裂原活化蛋白激酶（MAP激酶）的信号转导途径介导的。先前的遗传学分析表明，该途径在阴门前体细胞中的两个潜在靶标是两种新蛋白，即LIN-25和SUR-2。在本报告中，我们描述了对lin-25的进一步研究。遗传镶嵌分析的结果以及在异源启动子控制下表达lin-25的实验结果表明，lin-25在阴门诱导过程中的主要作用靶点是阴门前体细胞本身。我们制备了针对LIN-25的抗血清，并利用这些抗血清分析蛋白质表达模式。在阴门诱导之前和诱导过程中，LIN-25存在于所有六个前体细胞中，但随后局限于阴门谱系的细胞中。Ras/MAP激酶途径中的基因突变不影响表达模式，但在缺乏sur-2的情况下，LIN-25的积累减少。LIN-25的过表达不能挽救sur-2突变体的缺陷，这表明LIN-25和SUR-2可能共同发挥作用。LIN-25也在外侧皮下组织中表达。LIN-25的过表达破坏了外侧皮下细胞融合，这表明lin-25可能在秀丽隐杆线虫中调节细胞融合中发挥作用。
