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. 2017 Aug 16;18(8):1774. doi: 10.3390/ijms18081774

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Trimethylation of H3K36 by SETD2 is required for function of DNA repair system via homologous recombination (HR) repair and mismatch repair (MMR). HR repair of DNA double-strand breaks (DSBs) occurs with the help of Lens epithelium-derived growth factor p75 (LEDGF) that binds to H3K36me3 and allows recruitment of C-terminal binding protein interacting protein (CtIP) to the DSB sites. This further allows Replication Protein A (RPA) and RAD51 binding to damaged sites. In addition, H3K36me3 contributes to MMR via recruiting the mismatch recognition protein hMutSα onto chromatin. SETD2 inactivation results in the global reduction of the histone mark H3K36me3. This leads to deficiency in DNA repair systems which in turn contributes to genome instability. Blue DNA lines means DNA is repaired while Red DNA lines means DNA is not repaired.