Journal
DNA REPAIR
Volume 4, Issue 7, Pages 782-792Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2005.03.005
Keywords
homologous recombination; nonhomologous end joining; Fanconi anemia; DNA double-strand breaks; cell synchrony
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Funding
- NCI NIH HHS [CA89405] Funding Source: Medline
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Unrepaired DNA double-strand breaks (DSBs) produced by ionizing radiation (IR) are a major determinant of cell killing. To determine the contribution of DNA repair pathways to the well-established cell cycle variation in IR sensitivity, we compared the radiosensitivity of wild-type CHO cells to mutant lines defective in nonhomologous end joining (NHEJ). homologous recombination repair (HRR), and the Fanconi anemia pathway. Cells were irradiated with IR doses that killed similar to 90% of each asynchronous population. separated into synchronous fractions by centrifugal elutriation, and assayed for survival (colony formation). Wild-type cells had lowest resistance in early G 1 and highest resistance in S phase, followed by declining resistance as cells move into G2/M. In contrast, HR-defective cells (xrcc3 mutation) were most resistant in early G1 and became progressively less resistant in S and G2/M. indicating that the S-phase resistance in wild-type cells requires HRR. Cells defective in NHEJ (dna-pk(cs) mutation) were exquisitely sensitive in early G1. most resistant in S phase, and then somewhat less resistant in G2/M. Fancg mutant cells had almost normal IR sensitivity and normal cell cycle dependence. suggesting that Fancg contributes modestly to survival and in a manner that is independent of cell cycle position. Published by Elsevier B.V.
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