Irradiation of DNA by UV (ultraviolet light) causes lesions, such as cyclobutane-pyrimidine dimers or 6-4PPs (6-4 pyrimidine pyrimidone). The most common covalently linked adjoining pyrimidines are T-T (thymine dimers), T-C (thymine-cytosine dimers) and C-C (cytosine-cytosine dimers). T-T dimers cause kinks in the DNA strand that prevent both replication and transcription of that part of the DNA. Because they block DNA replication (and therefore prevent cells from reproducing), T-T dimers and other forms of UV damage cannot be inherited, and thus do not constitute mutations. Such kinds of DNA damage are known as premutational lesions because they prevent both transcription and replication of the genes in which they are present, and these lesions are fatal if they go uncorrected (Ref. 2).
References:
1.Photorepair prevents ultraviolet-induced apoptosis in human cells expressing the marsupial photolyase gene.
Chigancas V, Miyaji EN, Muotri AR, de Fatima Jacysyn J, Amarante-Mendes GP, Yasui A, Menck CF. Cancer Res. 2000 May 1; 60(9): 2458-63. 2.UV-induced DNA damage and repair: a review. Sinha RP, Hader DP. Photochem Photobiol Sci. 2002 Apr; 1(4): 225-36. Review. 3.Photoreactivation of UV-induced cyclobutane pyrimidine dimmers in the MFA2 gene of Saccharomyces cerevisiae. Morse NR, Meniel V, Waters R. Nucleic Acids Res. 2002 Apr 15; 30(8): 1799-807. 4.Chromatin structure modulates DNA repair by photolyase in vivo. Suter B, Livingstone-Zatchej M, Thoma F. EMBO J. 1997 Apr 15; 16(8): 2150-60.
|