Journal
JOURNAL OF RADIATION RESEARCH
Volume 62, Issue 1, Pages 25-33Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jrr/rraa095
Keywords
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Funding
- Japan Society for the Promotion of Science [22310033, 24310038, 19 K12318]
- Grants-in-Aid for Scientific Research [22310033] Funding Source: KAKEN
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The repair pathway choice for DNA double-strand breaks is dependent on cell cycle phases, with homologous recombination repair most active in the S phase; unexpectedly, significant homology directed repair activity was also observed during mitosis.
The choice of repair pathways of DNA double-strand breaks (DSBs) is dependent upon the cell cycle phases. While homologous recombination repair (HRR) is active between the S and G2 phases, its involvement in mitotic DSB repair has not been examined in detail. In the present study, we developed a new reporter assay system to detect homology directed repair (HDR), a major pathway used for HRR, in combination with an inducible DSB-generation system. As expected, the maximal HDR activity was observed in the late S phase, along with minimal activity in the G1 phase and at the G1/S boundary. Surprisingly, significant HDR activity was observed in M phase, and the repair efficiency was similar to that observed in late S phase. HDR was also confirmed in metaphase cells collected with continuous colcemid exposure. ChIP assays revealed the recruitment of RAD51 to the vicinity of DSBs in M phase. In addition, the ChIP assay for gamma-H2AX and phosphorylated DNA-PKcs indicated that a part of M-phase cells with DSBs could proceed into the next G1 phase. These results provide evidence showing that a portion of mitotic cell DSBs are undoubtedly repaired through action of the HDR repair pathway.
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