CHAPTER 11: The Role of Chromatin and Chromatin-modifying Enzymes in Regulating Nucleotide Excision Repair
Published:06 Dec 2021
Special Collection: 2021 ebook collection
K. Selvam, D. A. Plummer, K. A. Bohm, and J. J. Wyrick, in DNA Photodamage: From Light Absorption to Cellular Responses and Skin Cancer, ed. R. Improta and T. Douki, The Royal Society of Chemistry, 2021, pp. 252-270.
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Ultraviolet (UV) light induces helix-distorting photoproducts in DNA. These UV photoproducts must be rapidly repaired by the nucleotide excision repair (NER) pathway to prevent cell death or mutagenesis. In eukaryotic cells, the NER machinery must be able to detect and repair UV photoproducts embedded in chromatin. Past studies have shown that even the nucleosome, which comprises the lowest level of chromatin packaging, can inhibit the repair of UV photoproducts. However, a number of mechanisms are present in cells that can facilitate repair in chromatin, including histone post-translational modifications, such as lysine acetylation or methylation, or ATP-dependent chromatin remodeling. Here, we review our current understanding of how chromatin and chromatin modifications modulate NER of UV photoproducts.