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Studies on molecular mechanisms regulating the morphogenetic movement of the C.elegans vulva.

线虫外阴形态发生运动调控的分子机制研究。

基本信息

批准号：
15570174
负责人：
TAKAGI Shin
金额：
$ 2.37万
依托单位：
Nagoya University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15570174/
关键词：
C.elegans plexin semaphorin vulva morphogenesis 表皮形態形成

项目摘要

PLX-1 is a PlexinA transmembrane protein in C.elegans, and the transmembrane-type semaphorins, SMP-1,is a ligand for PLX-1. The SMP-1/PLX-1 system has been shown to be necessary for proper epidermal morphogenesis in the male tail and seam cells. Here we show that the SMP-1/PLX-1 system also regulates vulval morphogenesis. In plx-1 and smp-1 mutants, hermaphrodites sometimes exhibit a protruding vulva or multiple vulva-like protrusions. Throughout the vulval development of plx-1 and smp-1 mutants, the arrangement of vulval primordial cells is often disrupted. In the initial step of vulval morphogenesis, vulval precursor cells(VPCs) are generated normally but are subsequently arranged abnormally in mutants. Continuous observation revealed that plx-1 VPC fails to terminate longitudinal extension after making contact with neighbor VPCs. The arrangement defects of VPCs in plx-1 and smp-1 mutants are rescued by expressing the respective cDNA in VPCs. plx-1::egfp and smp-1::egfp transgenes are both expressed in all vulval primordial cells, including VPCs, throughout vulval development. We propose that the SMP-1/PLX-1 system is responsible for a cell contact-mediated stop signal for VPC extension. Analyses using cell fate-specific markers showed that the arrangement defects of VPCs also affect cell fate specification and cell lineages, but in a relatively small fraction of plx-1 mutants.

PLX-1是秀丽隐杆线虫中的丛蛋白A跨膜蛋白，而跨膜型信号蛋白（SMP-1）是PLX-1的配体。SMP-1/PLX-1系统已被证明是必要的适当的表皮形态发生在男性的尾巴和接缝细胞。在这里，我们表明，SMP-1/PLX-1系统也调节外阴形态发生。在plx-1和smp-1突变体中，雌雄同体有时表现出外阴突出或多个外阴样突起。在plx-1和smp-1突变体的整个外阴发育过程中，外阴原始细胞的排列经常被破坏。在外阴形态发生的初始阶段，外阴前体细胞（VPC）正常产生，但随后在突变体中排列异常。连续观察发现，plx-1 VPC在与相邻VPC接触后不能终止纵向延伸。plx-1和smp-1突变体中VPCs的排列缺陷通过在VPCs中表达相应的cDNA而被拯救。plx-1：：egfp和smp-1：：egfp转基因在整个外阴发育过程中均在所有外阴原始细胞（包括VPC）中表达。我们建议，SMP-1/PLX-1系统是负责细胞接触介导的停止信号VPC的延伸。使用细胞命运特异性标记物的分析表明，VPC的排列缺陷也影响细胞命运的规范和细胞谱系，但在一个相对较小的比例plx-1突变体。