| Project/Area Number |
16570165
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cell biology
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| Research Institution | National Institute for Basic Biology |
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Principal Investigator |
KAMADA Yoshiaki National Institute for Basic Biology, Division of Molecular and Cellular Biology, Research associate, 分子細胞生物学研究部門, 助手 (20291891)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | Nutrient starvation / autophagy / TOR / protein kinase / プロテインキナーゼ / 出芽酵母 / ストレス応答 |
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| Research Abstract |
Atg17 is a Atg1-binding protein which is essential for activation of Atg1. Biochemical characterization of Atg17 protein was performed in this project. As the result, it is found that Atg1-Atg17 association is regulated by Tor, and that this binding is necessary for autophagy induction.
Atg29 was identified as a novel protein involved in autophagy. We found that Atg29 binds to Atg17 and that it is phosphorylated by Atg1.
Tor signaling pathway also regulates actin organization. We found that a protein kinase Ypk2 is directly phosphorylated by Tor2 at the C-terminus. Ypk2 phosphorylation by Tor2 is essential for activation of Ypk2 and actin organization. We also isolated activated allele of Ypk2 (Ypk2-D239A), whose activity is Tor2-independently enhanced. YPK2-D239A can rescue the lethality of tor2 deletion mutant, suggesting that Ypk2 acts as a essential downsream of Tor signaling.
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