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Published online 5 March 2004

Nucleic Acids Research, 2004, Vol. 32, No. 4 1602-1609
© 2004 Oxford University Press

Processing of clustered DNA damage generates additional double-strand breaks in mammalian cells post-irradiation

Melanie Gulston, Catherine de Lara, Terry Jenner, Emma Davis and Peter O’Neill*

DNA Damage Group, MRC Radiation and Genome Stability Unit, Harwell, Didcot OX11 0RD, UK

*To whom correspondence should be addressed. Tel: +44 1235 841017; Fax: +44 1235 841200; Email: p.oneill{at}har.mrc.ac.uk

Clustered DNA damage sites, in which two or more lesions are formed within a few helical turns of the DNA after passage of a single radiation track, are signatures of DNA modifications induced by ionizing radiation in mammalian cells. Mutant hamster cells (xrs-5), deficient in non-homologous end joining (NHEJ), were irradiated at 37°C to determine whether any additional double-strand breaks (DSBs) are formed during processing of {gamma}-radiation-induced DNA clustered damage sites. A class of non-DSB clustered DNA damage, corresponding to ~30% of the initial yield of DSBs, is converted into DSBs reflecting an artefact of preparation of genomic DNA for pulsed field gel electrophoresis. These clusters are removed within 4 min in both NHEJ-deficient and wild-type CHO cells. In xrs-5 cells, a proportion of non-DSB clustered DNA damage, representing ~10% of the total yield of non-DSB clustered DNA damage sites, are also converted into DSBs within ~30 min post-{gamma} but not post-{alpha} irradiation through cellular processing at 37°C. That the majority of radiation-induced non-DSB clustered DNA damage sites are resistant to conversion into DSBs may be biologically significant at environmental levels of radiation exposure, as a non-DSB clustered damage site rather than a DSB, which only constitutes a minor proportion, is more likely to be induced in irradiated cells.


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