2016 Fiscal Year Final Research Report
Formation and organization of ER exit site
| Project/Area Number |
26840031
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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 | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | 小胞体 / 輸送小胞 / COPII / GTPaes |
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| Outline of Final Research Achievements |
COPII-coated vesicle carriers, which mediate transport of cargo molecules from the ER to the Golgi complex, are formed at specific domains of the ER membranes, called ER exit sites (ERESs). Regulation of Sar1 GTPase activity is an important process for COPII vesicle formation. Sec16 is essential for ER-Golgi transport and suggested to play a crucial role in ERES formation. Here I investigated Sec16 function and shed light on new mechanistic insights. I find that the N-terminal region of Sec16 can activates Sar1 GTPase. The domain for GTPase activation is identified in the N-terminal region and found to be required for Sec16 function in membrane association and ERES formation. Moreover, I report that the N-terminal region is able to facilitate COPII-mediated vesicle formation. These results provide novel regulatory mechanisms of how Sec16 organizes ERES and potentiates COPII action for vesicle formation.
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| Free Research Field |
細胞生物学
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