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. 2013 Aug 7;41(19):9006–9019. doi: 10.1093/nar/gkt688

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 8. — Model for chromatin remodelling at MFA2 during NER. Top panel. In the absence of UV histone H3 tails remain unacetylated and chromatin remains repressive. Middle Panel. After UV irradiation, the increased occupancy of Gcn5 that is mediated via the Rad7/Rad16 GG-NER complex is promoted by the presence of Htz1. This helps achieve enhanced acetylation levels on histone H3, which are critical for the specific chromatin setting required for optimal NER, so ensuring maximal binding of repair proteins, e.g. Rad14, to damaged DNA. This leads to efficient lesion removal. Lower Panel. Without Htz1 in these nucleosomes, the occupancy of Gcn5 and the acetylation levels on histone H3 are reduced. Therefore, the maximal binding of repair proteins to damaged DNA cannot be achieved and more CPDs remain unrepaired.