Analysis of Atg5 dependent and independent autophagy and induction mechanism of inflammation during bacterial infection.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25293370
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Morphological basic dentistry
• Research Institution: Kyoto University (2014-2015); Tokyo Medical and Dental University (2013)
• Principal Investigator: NAKAGAWA ICHIRO 京都大学, 医学(系)研究科(研究院), 教授 (70294113)
• Co-Investigator(Kenkyū-buntansha): Maruyama Fumito 京都大学, 大学院医学研究科, 准教授 (30423122)
• Co-Investigator(Renkei-kenkyūsha): NOZAWA TAKASHI 京都大学, 大学院医学研究科, 助教 (10598858)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: A群レンサ球菌 / xenophagy / オートファジー / Rabタンパク質 / 炎症

Outline of Final Research Achievements

Autophagy in mammalian cells not only supplies nutrients under starvation conditions but also protects against human diseases by selectively degrading aggregated proteins, damaged organelles, and invading microbes. Rab proteins are localized to distinct intracellular membranes and vesicles and function as molecular switches that alternate between two conformational states. We found that GcAV-regulating Rab proteins include Rab9A and Rab23, which are dispensable for starvation-induced autophagy. Autophagy involves highly conserved cellular machinery, has various physiological roles, and plays a role in immunity against intracellular pathogens. Our findings suggest that autophagy uses involves Rab proteins during distinct stages of development. Further studies examining autophagy during GAS infection will help define these detailed interactions between host cells and bacterial pathogens.

Free Research Field

細菌学