Nucleic Acids Research, 2003, Vol. 31, No. 15 4541-4552
© 2003 Oxford University Press
Roles of Saccharomyces cerevisiae DNA polymerases Pol
and Pol
in response to irradiation by simulated sunlight
1 CNRS-IC UMR 2027, Institut Curie, Bât. 110, Centre Universitaire, F-91405 Orsay, France, 2 Department of Genetics, Sankt-Petersburg State University, Sankt-Petersburg, 199034, Russia and 3 Laboratories of Molecular Genetics and Laboratory of Structural Biology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA
*To whom correspondence should be addressed. Tel: +33 1 69 86 71 87; Fax: +33 1 69 86 94 29; Email: evelyne.sage{at}curie.u-psud.fr
Sunlight causes lesions in DNA that if unrepaired and inaccurately replicated by DNA polymerases yield mutations that result in skin cancer in humans. Two enzymes involved in translesion synthesis (TLS) of UV-induced photolesions are DNA polymerase 
(Pol) and polymerase 
(Pol), encoded by the RAD30A and REV3 genes, respectively. Previous studies have investigated the TLS roles of these polymerases in human and yeast cells irradiated with monochromatic, short wavelength UVC radiation (254 nm). However, less is known about cellular responses to solar radiation, which is of higher and mixed wavelengths (310–1100 nm) and produces a different spectrum of DNA lesions, including Dewar photoproducts and oxidative lesions. Here we report on the comparative cytotoxic and mutagenic effects of simulated sunlight (SSL) and UVC radiation on yeast wild-type, rad30
, rev3 and rev3 rad30 strains. The results with SSL support several previous interpretations on the roles of these two polymerases in TLS of photodimers and (6–4) photoproducts derived from studies with UVC. They further suggest that Pol participates in the non-mutagenic bypass of SSL-dependent cytosine-containing Dewar photoproducts and 8-oxoguanine, while Pol is mainly responsible for the mutagenic bypass of all types of Dewar photoproducts. They also suggest that in the absence of Pol, Pol contributes to UVC- and SSL-induced mutagenesis, possibly by the bypass of photodimers containing deaminated cytosine.
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