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

PLX-1是线虫体内的PlexinA跨膜蛋白，跨膜型信号素SMP-1是PLX-1的配体。SMP-1/PLX-1系统被证明是雄性尾巴和缝隙细胞正常的表皮形态发生所必需的。在这里，我们发现SMP-1/PLX-1系统也调节外阴的形态发生。在plx-1和SMP-1突变体中，两性人有时会表现出一个突出的外阴或多个外阴样突起。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打乱。在外阴形态发生的最初阶段，外阴前体细胞(VPC)正常生成，但随后在突变体中出现异常排列。连续观察发现，PLX-1私有网络在与邻居私有网络接触后，无法终止纵向延伸。PLX-1和SMP-1突变体中的VPC排列缺陷可通过在VPC中表达相应的基因来挽救。在整个外阴发育过程中，PLX-1：：EGFP和SMP-1：：EGFP转基因均在包括VPC在内的所有外阴原始细胞中表达。我们认为SMP-1/PLX-1系统负责细胞接触介导的vPC延长的停止信号。使用细胞命运特异性标记的分析表明，VPC的排列缺陷也影响细胞命运规范和细胞谱系，但在PLX-1突变体中相对较小。

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.