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All eukaryotic cells manifest cell cycle delay after exposure to DNA damaging agents. It has been proposed that such cell cycle checkpoints may allow DNA repair but direct evidence of such activity during the radiation-induced G2 delay has been lacking. We report here that cells arrested in G2 by radiation (2-3 Gy) and etoposide incorporate bromodeoxyuridine (BrdU) at discrete foci in the nucleus. We detected G2 cells with CENP-F, a nuclear protein maximally expressed in G2. Caffeine and okadaic acid, both established radiosensitizers, inhibit the incorporation of BrdU in G2 cells. Radioresistant HT29 and OVCAR cells demonstrate BrdU foci formation more frequently during the G2 delay when compared to the more radiosensitive A2780 cell line. The repair foci formed during G2 may be followed through mitosis and observed in daughter cells in G1. Taken together, these observations are consistent with the detection of DNA repair activity during the radiation-induced G2 delay after relatively low doses of radiation.

Original publication

DOI

10.1038/sj.onc.1204445

Type

Journal article

Journal

Oncogene

Publication Date

14/06/2001

Volume

20

Pages

3486 - 3496

Keywords

Bromodeoxyuridine, Cell Cycle, Centromere, Chromosomal Proteins, Non-Histone, DNA Damage, DNA Repair, DNA, Neoplasm, Etoposide, Female, Flow Cytometry, G2 Phase, Gamma Rays, HeLa Cells, Humans, Kinetics, Microfilament Proteins, Ovarian Neoplasms, Radiation Tolerance, Tumor Cells, Cultured