Elucidation of the mechanism of lipidation of a ubiquitin-like protein that drives autophagosome formation

2016 Fiscal Year Final Research Report

• Project/Area Number: 26840017
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Structural biochemistry
• Research Institution: Tokyo Institute of Technology
• Principal Investigator: Nakatogawa Machiko 東京工業大学, 生命理工学院, JSPS特別研究員 (90402461)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: オートファジー / ユビキチン様タンパク質 / E2酵素 / 蛍光顕微鏡

Outline of Final Research Achievements

Autophagy is a lysosome/vacuole-mediated degradation system in eukaryotic cells, involved in various diseases such as neurodegenerative diseases, hepatic diseases, cancer, and diabetes. Formation of double-membrane vesicles “autophagosomes” that enwrap degradation targets is essential for autophagy. In this study, we revealed the localization of the autophagy-related protein Atg3 to autophagosome intermediates under autophagy-inducing conditions, and that the impairment of its localization results in inefficient autophagosome formation. Based on our results, we proposed the mechanism by which Atg3 participate in autophagosome formation.

Free Research Field

生物学