2010 Fiscal Year Final Research Report

Functional analysis of Rab33B in autophagy.

Research Project

Project/Area Number	21770198
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Cell biology
Research Institution	Tohoku University
Principal Investigator	ITOH Takashi Tohoku University, 大学院・生命科学研究科, 助教 (50373270)
Project Period (FY)	2009 – 2010
Keywords	タンパク質分解 / 膜輸送
Research Abstract	The direct interaction of Rab33B, a regulator of membrane trafficking, with Atg16L1, an essential factor for autophagy, suggests involvement of Rab33B in the regulation of autophagy. Here, I identified OATL1, an uncharacterized TBC protein, as an inactivation factor of Rab33B and addressed the function of Rab33B in autophagy to inactivate Rab33B by OATL1. Overexpression of OATL1, which would inactivate endogenous Rab33B, delayed autophagosomal maturation in MEF cells. On the other hand, overexpression of active-form mutant of Rab33B also delayed autophagosomal maturation. These results indicate that Rab33B plays a role in the fusion between autophagosomes and lysosomes, a later process of autophagy.

(5 results)