Pfeifer G P
Department of Biology, Beckman Institute of the City of Hope, Duarte, CA 91010, USA.
Photochem Photobiol. 1997 Feb;65(2):270-83. doi: 10.1111/j.1751-1097.1997.tb08560.x.
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.
环丁烷嘧啶二聚体和（6-4）光产物是紫外线B（UVB）和紫外线C（UVC）照射在DNA中产生的两类主要损伤。它们沿基因的分布取决于核苷酸序列。在体内，这些损伤在特定位点的频率受核小体和其他DNA结合蛋白的调节。紫外线光产物的修复取决于待修复序列的转录状态和染色质环境。紫外线诱导的DNA光损伤的形成是导致突变和皮肤癌发生的原因。为了理解紫外线诱变的机制，了解这些损伤是如何形成的、通过哪些细胞途径进行修复以及DNA聚合酶如何处理它们是很重要的。
