| Budget Amount *help |
¥16,640,000 (Direct Cost: ¥12,800,000、Indirect Cost: ¥3,840,000)
Fiscal Year 2016: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2015: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
Fiscal Year 2014: ¥10,920,000 (Direct Cost: ¥8,400,000、Indirect Cost: ¥2,520,000)
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| Outline of Final Research Achievements |
DNA double-strand breaks caused by ionizing radiation result in an activation of ATM-dependent DNA damage signaling pathway. While most of DNA breaks are amendable, unreparable and residual breaks amplify DNA damage signal, which will be transmitted through mitosis. In the present study, it was aimed to identify epigenetic marks associated with DNA damage signal transmission. Analyses using immunofluorescence revealed that histone modifications, such as methylation, acetylation, and ubiquitination, might not be involved in the process, whereas phosphorylation of histone H2AX remained on damaged chromosomes. In addition, localization of MDC1 on damaged chromosomes was detected during mitosis. These results indicate that epigenetic modification of H2AX is critical for the transmission of amplified DNA damage signal through cell division.
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