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- Title
Signatures of DNA double strand breaks produced in irradiated G1 and G2 cells persist into mitosis.
- Authors
KATO, TAKAMITSU A.; OKAYASU, RYUICHI; BEDFORD, JOEL S.
- Abstract
We have observed that some of the DNA damage or damage product caused by irradiation of interphase cells persisted throughout the cell cycle, and resulted in the expression of γ-H2AX foci on the mitotic chromosomes. These mitotic expressions of damage after γ-irradiation of G1 or G2 phase cells were compared in wild-type CHO and their DNA repair deficient XR-1 and UV-1 cells. γ-H2AX foci were located on one of the chromatids or on both chromatids as isolocus paired foci. DNA double strand break (DSB) repair deficient XR-1 cells exhibited greater persistence of γ-H2AX foci than wild-type cells when irradiated at G1 phase. Delayed subculture after irradiation significantly reduced the persistence of damage in mitotic cells and the radiosensitivity in wild-type cells, but this was not the case for XR-1 cells. Interestingly, UV and crosslinking agents sensitive UV-1 cells which show similar sensitivity to γ-irradiation as wild-type cells by γ-irradiation, exhibited significantly higher γ-H2AX persistence at mitosis when they were irradiated in G1-phase but not in G2-phase. One interpretation of this is that it is due to DNA damage accumulating at stalled replication forks. As in wild type cells, in delayed subculture after γ-ray exposure of UV-1 cells, a reduced number of foci was also seen. Our results suggest that the persistence of γ-H2AX foci does not always correspond with the radiosensitivities of cells, but rather depends on cells' ability to repair the different kinds of DNA damages. J. Cell. Physiol. 219: 760–765, 2009. © 2009 Wiley-Liss, Inc.
- Subjects
SUBCULTURES; IRRADIATION; CELLS; CELL cycle; CHROMOSOMES; DNA repair
- Publication
Journal of Cellular Physiology, 2009, Vol 219, Issue 3, p760
- ISSN
0021-9541
- Publication type
Article
- DOI
10.1002/jcp.21726