2011 Fiscal Year Final Research Report
A study of epidermal morphogenesis regulated by semaphorin signaling
Project/Area Number |
21370097
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Developmental biology
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Research Institution | Nagoya University |
Principal Investigator |
TAKAGI Shin 名古屋大学, 理学研究科, 准教授 (90171420)
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Project Period (FY) |
2009 – 2011
|
Keywords | セマフォリン / 表皮 / 形態形成 / 線虫 / TOR / 器官形成 |
Research Abstract |
The target of rapamycin (TOR) resides in the two functionally distinct complexes TORC1 and TORC2, which are defined by their adaptors Raptor and Rictor, respectively. How the formation of the two TORCs is orchestrated remains unclear. Through our study in C. elegans, we demonstrated the control of TOR partnering by semaphorin-plexin signaling in vivo. In semaphorin and plexin mutants, TOR-Raptor association decreases whereas TOR-Rictor association increases, concomitantly with TORC1 down- and TORC2 up-regulation. Epidermal defects in semaphorin and plexin mutants are suppressed by inhibiting TORC2 or reinforcing TORC1 signaling. Conversely, inhibition of TORC1 signaling phenocopies semaphorin and plexin mutants. Our results indicate that TORC formation is a singularly important step in semaphorin signaling that culminates in diverse outcomes including TORC1-promoted mRNA translation and TORC2-regulated cytoskeletal remodeling.
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[Remarks] 「セマフォリンによる細胞の形の制御機構解明」 名大トピックス No.226 2012年3月15日発行
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[Remarks] 「細胞変形、仕組み解明」 日経産業新聞2011年12月2日
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[Remarks] 「動物細胞の形制御 分子の仕組み解明」日刊工業新聞2011年10月18日 3面
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[Remarks] 「細胞の伸び仕組み解明」中日新聞 朝刊 2011年9月28日 3面