2010 Fiscal Year Final Research Report
Molecular mechanisms of DNA damage tolerance for chronic low-dose UV light
| Project/Area Number |
20370002
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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 |
Genetics/Genome dynamics
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| Research Institution | Osaka University |
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Principal Investigator |
HISHIDA Takashi Osaka University, 微生物病研究所, 准教授 (60335388)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 分子遺伝 / DNA損傷 / 紫外線 |
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| Research Abstract |
Uultraviolet (UV) light in from sunlight, which is a primary significant environmental cause of DNA damage, that, if left unrepaired, can lead to cancer- and other disease-causing mutations. In nature, organisms are exposed to chronic low-dose UV (CLUV) as opposed to the acute high doses common to laboratory experiments. Here we examine the response of yeast cells to CLUV and identify a key role for the RAD6 error-free postreplication repair (RAD6 error-free PRR) pathway in promoting cell growth and survival. Notably, we showed that the error-free PRR pathway is specifically important during chronic low-dose UV exposure to prevent counter-productive DNA checkpoint activation and allow cells to proliferate normally. Furthermore, we also showed that suppression of homologous recombination (HR) in PRR-deficient cells by Srs2 is required for checkpoint activation and checkpoint maintenance during CLUV irradiation.
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