2004 Fiscal Year Final Research Report Summary
Cell cycle checkpoint control
| Project/Area Number |
15370089
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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 |
Cell biology
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| Research Institution | NAGOYA CITY UNIVERSITY |
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Principal Investigator |
MURAKAMI Hiroshi Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (80262020)
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| Project Period (FY) |
2003 – 2004
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| Keywords | cell cycle / checkpoint / meiosis / double strand breaks / DNA replication / recombination / rad3 / cdsl |
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| Research Abstract |
During meiosis, high levels of recombination initiated by DNA double-strand breaks (DSBs) occur only after DNA replication. How DSB formation is coupled to DNA replication is unknown, however. We examined several DNA replication proteins for a role in this coupling in Schizosaccharomyces pombe and now show that ribonucleotide reductase (RNR), the rate-limiting enzyme of deoxyribonucleotide synthesis and the target of the DNA synthesis inhibitor hydroxyurea (HU), is indirectly required for DSB formation linked to DNA replication. In cells in which the function of the DNA replication checkpoint proteins Rad1p, Rad3p, Rad9p, Rad17p, Rad26p, Hus1p, or Cdslp was compromised, however, DSB formation occurred at similar frequencies in the absence or presence of HU. The DSBs in the HU-treated mutant cells occurred at normal sites and were associated with recombination. In addition, Cdc2p is apparently not involved in this process. We propose that the sequence of meiotic S phase and initiation of recombination is coordinated by DNA replication checkpoint proteins.
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