2004 Fiscal Year Final Research Report Summary
Multifunctional molecular switch essential for cell morphogenesis
| Project/Area Number |
14380325
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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 |
Molecular biology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OHYA Yoshikazu University of Tokyo, Grad. Schl. Frontier Sci., Professor, 大学院・新領域創成科学研究科, 教授 (20183767)
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| Co-Investigator(Kenkyū-buntansha) |
SONOIKE Kintake University of Tokyo, Grad. Schl. Frontier Sci., Associate Professor, 大学院・新領域創成科学研究科, 助教授 (30226716)
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| Project Period (FY) |
2002 – 2004
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| Keywords | cell wall / yeast / cell cycle / checkpoint / polarized growth / cyclin / dynactin / glucan |
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| Research Abstract |
The coordination of cell cycle events during cell proliferation is attained, in part, through surveillance systems. In the budding yeast Saccharomyces cerevisiae, cell cycle progression is restrictively regulated and some events during cell cycle are regulated by the checkpoints monitoring DNA damage, DNA replication, integrity of the spindle, spindle positioning and cell morphogenesis. It still remained unclear whether all of the checkpoint controls have been identified.
Here we found that a novel checkpoint exists to couple cell wall remodeling with spindle formation. fks1 mutants defective in 1,3-β-glucan synthase activity failed to form a mature bud. Surprisingly, these cells arrested with post-replicative DNA but quite low level of Clb2p, and without forming bipolar spindles. We found that wac1 (wall-checkpoint defective) mutation that abolished this arrest caused the accumulation of Clb2p and CLB2 mRNA and leaded to formation of bipolar spindles despite glucan-synthesis perturbation. These results indicate the existence of a novel checkpoint mechanism to coordinate entry into mitosis, and suggest that Wac1p is required to achieve this checkpoint function through a transcriptional regulation of CLB2. Furthermore, we revealed that WAC1 was identical with ARP1 (actin-related protein). Arp1p, Nip100p and Jnm1p, which are components of the dynactin complex, are required to achieve the G2 arrest while keeping cells highly viable. These results indicate that the dynactin complex have a regulatory role in the novel checkpoint to monitor cell wall synthesis.
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