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| The EMBO Journal
(1999) 18, 6585–6598, doi:10.1093/emboj/18.23.6585 |
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| Light and dark in chromatin repair: repair of UV-induced DNA lesions by photolyase and nucleotide excision repair |
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| Fritz Thoma |
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Institut für Zellbiologie, ETH-Zürich, Hönggerberg, CH-8093 Zürich, Switzerland To whom correspondence should be addressed Fritz Thoma, thoma@cell.biol.ethz.ch Received 20 July 1999; Revised 30 September 1999; Accepted 4 October 1999. |
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| Abstract |
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| Nucleotide excision repair (NER) and DNA repair by photolyase in the presence of light (photoreactivation) are the major pathways to remove UV-induced DNA lesions from the genome, thereby preventing mutagenesis and cell death. Photoreactivation was found in many prokaryotic and eukaryotic organisms, but not in mammals, while NER seems to be universally distributed. Since packaging of eukaryotic DNA in nucleosomes and higher order chromatin structures affects DNA structure and accessibility, damage formation and repair are coupled intimately to structural and dynamic properties of chromatin. Here, I review recent progress in the study of repair of chromatin and transcribed genes. Photoreactivation and NER are discussed as examples of how an individual enzyme and a complex repair pathway, respectively, access DNA lesions in chromatin and how these two repair processes fulfil complementary roles in removal of UV lesions. These repair pathways provide insight into the structural and dynamic properties of chromatin and suggest how other DNA repair processes could work in chromatin. |
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| Keywords: chromatin, DNA repair, nucleotide excision repair, photolyase, transcription |
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