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lin-25,一种秀丽隐杆线虫中诱导阴门所必需的基因。

lin-25, a gene required for vulval induction in Caenorhabditis elegans.

作者信息

Tuck S, Greenwald I

机构信息

Department of Molecular Biology, Princeton University, New Jersey 08544.

出版信息

Genes Dev. 1995 Feb 1;9(3):341-57. doi: 10.1101/gad.9.3.341.

DOI:10.1101/gad.9.3.341
PMID:7867931
Abstract

During vulval development in the Caenorhabditis elegans hermaphrodite, the fates of six vulval precursor cells (VPCs) are influenced by distinct cell signaling events. In one event, a somatic gonadal cell, the anchor cell, induces the three nearest VPCs to adopt vulval cell fates. In another event, lateral signaling between adjacent VPCs specifies one of two different vulval fates, 1 degrees and 2 degrees. Induction of vulval fates by the anchor cell is mediated by a signal transduction pathway involving let-60 Ras, lin-45 Raf, and mpk-1/sur-1 MAP kinase, whereas lateral signaling is mediated by lin-12. We have shown that the mutant phenotype of lin-25, a gene required for VPC fate specification, results from a defect in vulval induction. Genetic epistasis experiments indicate that lin-25 is required in the inductive signaling pathway downstream of let-60 Ras and the Raf/MAP kinase cascade. A decrease in induction also appears to decrease lateral signaling. We have cloned and sequenced the lin-25 gene and shown that it encodes a novel protein that may be a target of the mpk-1/sur-1 MAPK.

摘要

在秀丽隐杆线虫雌雄同体的外阴发育过程中,六个外阴前体细胞(VPC)的命运受到不同细胞信号事件的影响。在一个事件中,一个体细胞性腺细胞,即锚定细胞,诱导三个最接近的VPC采用外阴细胞命运。在另一个事件中,相邻VPC之间的侧向信号指定了两种不同外阴命运中的一种,即1级和2级。锚定细胞对外阴命运的诱导是由一个信号转导途径介导的,该途径涉及let-60 Ras、lin-45 Raf和mpk-1/sur-1丝裂原活化蛋白激酶,而侧向信号是由lin-12介导的。我们已经表明,lin-25(VPC命运指定所需的一个基因)的突变表型是由外阴诱导缺陷导致的。遗传上位性实验表明,lin-25在let-60 Ras下游的诱导信号通路以及Raf/丝裂原活化蛋白激酶级联反应中是必需的。诱导的减少似乎也会降低侧向信号。我们已经克隆并测序了lin-25基因,并表明它编码一种可能是mpk-1/sur-1丝裂原活化蛋白激酶靶标的新型蛋白质。

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lin-25, a gene required for vulval induction in Caenorhabditis elegans.lin-25,一种秀丽隐杆线虫中诱导阴门所必需的基因。
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