title: C. elegans PlexinA PLX-1 mediates a cell contact-dependent stop signal in vulval precursor cells.
abstract: PLX-1 is a PlexinA transmembrane protein in Caenorhabditis elegans, and the transmembrane-type semaphorin, 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 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 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.
authors.affiliation: Division of Biological Science, Nagoya University Graduate School of Science, Furo-cho, Chikusa-ku, Nagoya 464-8602, Japan.
authors.forename: Zhicen
authors.initials: Z
authors.lastname: Liu
authors.forename: Takashi
authors.initials: T
authors.lastname: Fujii
authors.forename: Akira
authors.initials: A
authors.lastname: Nukazuka
authors.forename: Rie
authors.initials: R
authors.lastname: Kurokawa
authors.forename: Motoshi
authors.initials: M
authors.lastname: Suzuki
authors.forename: Hajime
authors.initials: H
authors.lastname: Fujisawa
authors.forename: Shin
authors.initials: S
authors.lastname: Takagi
mesh_terms: D000818:Animals; D030801:Animals, Genetically Modified; D017173:Caenorhabditis elegans / Q000196:embryology*; D029742:Caenorhabditis elegans Proteins / Q000378:metabolism*; D005835:Genitalia / Q000166:cytology / Q000196:embryology*; D049452:Green Fluorescent Proteins; D018613:Microscopy, Confocal; D009024:Morphogenesis; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*; D039961:Semaphorins / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism*; D019076:Transgenes / Q000235:genetics
chemical_list: D029742:Caenorhabditis elegans Proteins; D009419:Nerve Tissue Proteins; D011956:Receptors, Cell Surface; D039961:Semaphorins; C485184:enhanced green fluorescent protein; C492117:plx-1 protein, C elegans; D049452:Green Fluorescent Proteins