| First Author | van Zeeland AA | Year | 2005 |
| Journal | Mutat Res | Volume | 577 |
| Issue | 1-2 | Pages | 170-8 |
| PubMed ID | 15949822 | Mgi Jnum | J:100610 |
| Mgi Id | MGI:3588931 | Doi | 10.1016/j.mrfmmm.2005.03.018 |
| Citation | van Zeeland AA, et al. (2005) Transcription-coupled repair: impact on UV-induced mutagenesis in cultured rodent cells and mouse skin tumors. Mutat Res 577(1-2):170-8 |
| abstractText | UV-induced cyclobutane pyrimidine dimers (CPDs) are removed with accelerated speed from the transcribed strand of expressed genes in cultured mammalian cells by a process called transcription-coupled repair (TCR). It has been previously shown that this phenomenon has consequences for the molecular nature of the mutations induced by UV-light. Here, we review these data and show that TCR has not only a clear impact on UV-induced mutations in cultured mammalian cells but also on genes involved in tumor formation in the skin of UV-exposed mice. Mutations observed in the p53 gene in UV-induced squamous cell carcinoma are predominantly found at sites of dipyrimidines in the non-transcribed strand. In contrast, in UVC-irradiated Csb(-/-) Chinese hamster cells and in UVB-induced tumors in the Csb(-/-) mouse, almost all mutations are at positions of dipyrimidine sites in the transcribed strand of the mutated gene. Csb(-/-) mice appear to be susceptible to UVB-induced skin cancer in contrast to the human CSB patients. We speculate that the UVB-induced cancer susceptibility of Csb(-/-) mice is related to the absence of TCR as well as to a lack of a compensating global genome repair system for CPDs in mice. |
