Analysis of activation mechanism and physiological function of ARL family small GTPases

2017 Fiscal Year Final Research Report

• Project/Area Number: 26291038
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Cell biology
• Research Institution: Meiji Pharmaceutical University (2015-2017); The University of Tokyo (2014)
• Principal Investigator: Kontani Kenji 明治薬科大学, 薬学部, 教授 (30302615)
• Co-Investigator(Kenkyū-buntansha): 荒木 信 明治薬科大学, 薬学部, 助教 (20552904) ; 福山 征光 東京大学, 薬学研究科(研究院), 助教 (20422389) ; 齋藤 康太 東京大学, 薬学研究科(研究院), 助教 (60549632)
• Co-Investigator(Renkei-kenkyūsha): Katada Toshiaki 東京大学, 大学院薬学系研究科, 教授 (10088859)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 低分子量Gタンパク質 / リソソーム / エンドサイトーシス / 一次繊毛 / マウス / 胚発生 / 卵黄嚢内胚葉

Outline of Final Research Achievements

In this study, we clarified that the ARL family small GTPase ARL8b is necessary for normal growth and brain development of mouse embryos. ARL8b was found to be important for lysosomal degradation of maternally derived protein components incorporated in the visceral yolk sac endoderm, and the functional deficiency of ARL8b in the visceral yolk sac endoderm caused a reduction in the amount of amino acids in the embryo proper and a failure of embryonic growth. We also found that ARL8b may be involved in the regulation of BMP signaling in embryonic brain development.

Free Research Field

生化学、細胞生物学