| Project/Area Number |
25450516
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Applied molecular and cellular biology
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| Research Institution | Hiroshima University |
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Principal Investigator |
Mizuta Keiko 広島大学, 生物圏科学研究科, 名誉教授 (40166012)
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| Co-Investigator(Kenkyū-buntansha) |
FUNATO KOUICHI 広島大学, 大学院生物圏科学研究科, 准教授 (30379854)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | リボソーム生合成 / 小胞輸送 / 核小体 / 核膜 / 酵母 / 分泌経路 / シグナル伝達 / Rrs1 / 出芽酵母 / Arp2/3複合体 |
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| Outline of Final Research Achievements |
Secretory defects cause transcriptional repression of both ribosomal RNA and ribosomal protein genes in Saccharomyces cerevisiae. Rrs1 and Ebp2, ribosome biogenesis factors, are involved in the signaling pathway induced by secretory defects. We found that disruption of all four genes encoding GSK-3 homologs, especially Mck1, diminished the transcriptional repression of ribosomal protein genes in response to secretory defects. We showed that Rrs1 interacts with Arc35, a component of Arp2/3 complex and that Arc35 was involved in the secretory response via regulation of both actin and microtubule kinetochore.
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