2004 Fiscal Year Final Research Report Summary
Studies on molecular mechanisms regulating the morphogenetic movement of the C.elegans vulva.
| Project/Area Number |
15570174
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Developmental biology
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| Research Institution | Nagoya University |
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Principal Investigator |
TAKAGI Shin Nagoya University, Graduate School of Science, Associate Professor, 大学院・理学研究科, 助教授 (90171420)
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| Project Period (FY) |
2003 – 2004
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| Keywords | C.elegans / plexin / semaphorin / vulva / morphogenesis |
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| Research Abstract |
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.
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