2013 Fiscal Year Final Research Report
Molecular mechanisms of primary ciliary resorption and cilia-dependent cell cycle regulation.
| Project/Area Number |
23770136
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | Tokyo Women's Medical University (2012-2013)
Akita University (2011) |
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Principal Investigator |
SAITO Masaki 東京女子医科大学, 医学部, 助教 (50400271)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 一次線毛 / 細胞周期 / 細胞質ダイニン軽鎖 / アクチン重合 / エンドソーム形成 / 低分子量Gタンパク質 |
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| Research Abstract |
Primary cilia are nonmotile sensory organelles presented during the G0 phase of many cell types, and act as cellular antennae to receive a variety of environmental stimuli. Disruption of cilia function results in numerous human diseases and genetic disorders collectively called 'ciliopathies'. Although primary cilia are essential for sensing, little is known about the cellular machinery controlling the resorption of cilia. I previously showed that phosphorylation of Tctex-1, one of a light chain of cytoplasmic dynein complex, played an important role in resulting primary ciliary resorption. In the present study, I further suggested that Tctex-1 regulated primary ciliary resorption and cell cycle reentry through actin polymerization and endosome formation. Clathrin, a molecule involved in endosome formation, was distributed on periciliary region.
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