| Project/Area Number |
21510228
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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 |
Living organism molecular science
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| Research Institution | Yokohama City University |
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Principal Investigator |
KAWASAKI Hiroshi 横浜市立大学, 大学院・生命ナノシステム科学研究科, 准教授 (70169704)
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| Co-Investigator(Renkei-kenkyūsha) |
AKIMOTO Kazunori 横浜市立大学, 大学院・医学研究科, 助教 (70285104)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | プロテオミクス / タンパク質 / 複合体 / 細胞極性 / 翻訳後修飾 |
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| Research Abstract |
Cell polarization is a fundamental process by which cells establish asymmetry along a defined axis at a specific time point. The polarization generally occurs by an asymmetric distribution of specific proteins, nucleic acid or organelles in response to spatial cues. In the budding yeast Saccharomyces cerevisiae, such polarization induces asymmetric growth to form a bud which becomes the daughter cell. The deletion of BUD32 causes a random budding specifically in diploid cells. Bud32p, an atypical kinase, is involved in a signaling cascade of Sch9p kinase, a yeast homolog of Akt/PKB. In this study, we revealed that the Bud32 complex is involved in bipolar budding by regulating the localization of Bud9p. The kinase activity of Bud32p, which is essential for the functions of the EKC/KEOPS complex, was also required for bipolar bud site selection. However, the mutation of Bud32p at the phosphorylation site by Sch9p did not affect bipolar budding. BUD9 was necessary for random budding in the each deletion mutant of EKC/KEOPS components. The asymmetric localization of Bud9p was dependent on the complex, but Bud8p and Rax2p were not. RAX2 was genetically upstream of EKC/KEOPS genes for the regulation of bipolar budding. Split-GFP analysis revealed that Bud9p physically interacted with Rax2p at the birth scar in budded mother cells. These observations suggest that the interaction of Rax2p with Bud8p and Bud9p may contribute to the translocation of bipolar landmarks to the correct sites. We concluded that the EKC/KEOPS complex is specifically involved in the regulation of Bud9p localization downstream of Rax1p/Rax2p.
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