Elucidation of the regulatory mechanisms by phosphorylation-dephosphorylation that supports ER-to-Golgi vesicular traffic

2023 Fiscal Year Final Research Report

• Project/Area Number: 19K06655
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 44010:Cell biology-related
• Research Institution: The University of Tokyo
• Principal Investigator: Sato Ken 東京大学, 大学院総合文化研究科, 教授 (00303602)
• Project Period (FY): 2019-04-01 – 2024-03-31
• Keywords: 小胞輸送 / リン酸化 / COPII / 小胞体

Outline of Final Research Achievements

In this study, using vesicular transport between the endoplasmic reticulum and Golgi apparatus in budding yeast as a model system, we focused on phosphorylation and dephosphorylation of factors involved in this reaction and analyzed how transport reactions and related organelle formation are regulated and controlled. We found that the T21 residue of the COPII coat subunit is dephosphorylated by PP2A phosphatase. We also showed that phosphorylation of Sec16, which is involved in the formation of the ER exit site, is not functionally essential, and that Sec16 functions in concert with Sed4, which localizes to the ER membrane.

Free Research Field

細胞内輸送

Academic Significance and Societal Importance of the Research Achievements

真核細胞に普遍的に備わる小胞輸送と呼ばれる物質輸送の仕組みについて、特に小胞体からゴルジ体への小胞輸送反応に焦点をあて、その制御機構の一端を明らかにした。小胞輸送反応は他領域にも広く関わる細胞の基礎現象であるため、例えばこれまで原因が不明であった疾患の原因が小胞輸送機能の損傷にあるものが最近続々と報告されてきている。そのため、小胞輸送の仕組みを明らかにすることは、現代細胞生物学の重要なテーマであると同時に、創薬や疾患治療にも大きく寄与するものである。