Summary
Ultraviolet radiation is a powerful mutagen in eukaryotes and prokaryotes due to its ability to produce premutational lesions of DNA. Of the damage induced by UV-irradiation of DNA at 260 nm, the cyclobutane-type dipyrimidine and the pyrimidine-pyrimidine (6–4) lesions at sites of adjacent pyrimidines are principal cause of mutations. These bulky lesions greatly modify the structure and function of DNA and cause block of DNA replication and cellular death. Prokaryotic and eukaryotic cells are able to repair the DNA lesions as for example the UV-induced pyrimidine dimers. For example, in E.coli, a set of repair enzymes (uvr A,B,C) recognize and eliminate the length of structurally altered DNA, so that resynthesis of DNA can proceed. Thus, the cell survives unmutated to the DNA damage. If the DNA damage is unrepaired, mutations are fixed thanks to a complex interplay of factors e.g. the site of DNA lesion, the replication machinery and, at least in E.coli, a few UV-inducible cell functions.
This paper reviews the mechanisms of UV mutagenesis in E.coli and mammalian cells together with the qualitative and quantitative analysis of UV-induced mutations.
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Quinto, I., Mallardo, M., Ruocco, M.R., Arcucci, A., Scala, G. (1991). Ultraviolet Mutagenesis. In: Grandolfo, M., Rindi, A., Sliney, D.H. (eds) Light, Lasers, and Synchrotron Radiation. NATO ASI Series, vol 242. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0661-8_20
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