| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2010: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2009: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2008: ¥7,280,000 (Direct Cost: ¥5,600,000、Indirect Cost: ¥1,680,000)
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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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