Koga M, Ohshima Y
Department of Biology, Faculty of Science, Kyushu University, Fukuoka, Japan.
Development. 1995 Aug;121(8):2655-66. doi: 10.1242/dev.121.8.2655.
The let-23 receptor tyrosine kinase gene is required for vulval induction and larval survival in the nematode Caenorhabditis elegans. We carried out genetic mosaic analyses of the let-23 gene function by using the cloned let-23 and ncl-1 genes. The wild-type let-23 gene was required in a vulval precursor cell to adopt the 1 degree vulval fate in animals carrying a let-23 vulvaless or lethal chromosomal mutation. In almost all the animals, vulval precursor cells adjacent to a 1 degree fate cell were induced to the 2 degrees vulval fate regardless of the let-23 genotypes. These findings indicate that the vulval induction signal from an anchor cell induces a vulval precursor cell to adopt the 1 degree fate through LET-23, and then a 1 degree fate cell induces adjacent cells to adopt the 2 degrees fate, for which LET-23 is not required. Foci of lethality of the let-23 (mn23) mutation were found in ABal and ABplp lineages.
在秀丽隐杆线虫中,let-23受体酪氨酸激酶基因对于外阴诱导和幼虫存活是必需的。我们通过使用克隆的let-23和ncl-1基因对let-23基因功能进行了遗传镶嵌分析。在携带let-23无外阴或致死性染色体突变的动物中,野生型let-23基因对于外阴前体细胞采用1级外阴命运是必需的。在几乎所有动物中,无论let-23基因型如何,与1级命运细胞相邻的外阴前体细胞都会被诱导为2级外阴命运。这些发现表明,来自锚定细胞的外阴诱导信号通过LET-23诱导外阴前体细胞采用1级命运,然后1级命运细胞诱导相邻细胞采用2级命运,而这一过程不需要LET-23。在ABal和ABplp谱系中发现了let-23(mn23)突变的致死位点。