| Project/Area Number |
10460044
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
応用微生物学・応用生物化学
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MIYAKAWA Tokichi Hiroshima University, Graduate School of Advanced Sciences of Matter, Professor, 大学院・先端物質科学研究科, 教授 (10116676)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUTA Keiko Hiroshima University, Faculty of Applied Bioscience, Professor, 生物生産学部, 教授 (40166012)
HIRATA Dai Hiroshima University, Graduate School of Advanced Sciences of Matter, Associate Professor, 大学院・先端物質科学研究科, 助教授 (30243603)
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| Project Period (FY) |
1998 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥12,700,000 (Direct Cost: ¥12,700,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2000: ¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1999: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 1998: ¥4,900,000 (Direct Cost: ¥4,900,000)
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| Keywords | Ca^<2+> signaling / Saccharomyces cerevisiae / Calcineurin / Cell cycle / Ca^<2+>シグナル / カルシニューリンニューリン / MAPキナーゼ / カルシウム / Ca^<2+> / チェックポイント |
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| Research Abstract |
We investigated molecular mechanism of G2/M cell cycle regulation by Ca^<2+> signal in Saccharomyces cerevisiae. We isolated mutants with a defect in the Ca^<2+> signaling pathway linked to cell cycle regulation. The mutants were classified to 14 complementation groups.
(1) csz7 mutant was analyzed in detail. The scz7 mutation was identified as an allele of MCK1 that encodes a GSK-3 family protein kinase highly conserved among eukaryotes. It was found that Mck1 was involved in the Ca^<2+>-induced destabilization of Hsl1, Negative regulator of Swe1 through the ubiquitin-proteasome pathway. We further revealed the detailed mechanism by which Hsl1 abundance is regulated.
(2) scz6 mutant was analyzed in detail. The scz6 mutation was identified as an allele of PKC1 that encodes a unique protein kinase C in the yeast. Interestingly, the scz6 mutation suppressed Ca^<2+> sensitive growth and Ca^<2+>-induced polarized bud growth, but not G2 cell cycle delay. We found a novel pathway of Pkc1, in which Pkc1 plays an important role in the regulation of the transcription of SWE1 And the G1 cyclin CLN1, in addition to the previously characterized pathway that activates the Mpk1 MAP kinase pathway. The transcription factor Swi4 was implicated in the transcriptional regulation of CLN1 and SWE1.
scz5 mutant was analyzed in detail. The scz5 mutation was identified as an allele of PDR5 that encodes an ABC transporter implicated in multidrug resistance in the yeast. Pdr5 was suggested to be responsible for Ca^<2+> uptake.
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