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Cyclobutane pyrimidine dimers and (6-4) photoproducts are the two major classes of lesions produced in DNA by UVB and UVC irradiation. Their distribution along genes is nucleotide sequence-dependent. In vivo, the frequency of these lesions at specific sites is modulated by nucleosomes and other DNA binding proteins. Repair of UV photoproducts is dependent on the transcriptional status of the sequences to be repaired and on the chromatin environment. The formation of DNA photolesions by UV light is responsible for the induction of mutations and the development of skin cancer. To understand the mechanisms of UV mutagenesis, it is important to know how these lesions are formed, by which cellular pathways they are repaired and how they are dealt with by DNA polymerases.
Gerd P. Pfeifer (Sat,) studied this question.