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  • Title: Signatures of DNA double strand breaks produced in irradiated G1 and G2 cells persist into mitosis.
    Author: Kato TA, Okayasu R, Bedford JS.
    Journal: J Cell Physiol; 2009 Jun; 219(3):760-5. PubMed ID: 19206160.
    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 gamma-H2AX foci on the mitotic chromosomes. These mitotic expressions of damage after gamma-irradiation of G1 or G2 phase cells were compared in wild-type CHO and their DNA repair deficient XR-1 and UV-1 cells. gamma-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 gamma-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 gamma-irradiation as wild-type cells by gamma-irradiation, exhibited significantly higher gamma-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 gamma-ray exposure of UV-1 cells, a reduced number of foci was also seen. Our results suggest that the persistence of gamma-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. (c) 2009 Wiley-Liss, Inc.
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