A histone H3K36 chromatin switch coordinates DNA double-strand break repair pathway choice

Chen-Chun Pai, Rachel S. Deegan, Lakxmi Subramanian, Csenge Gal, Sovan Sarkar, Elizabeth J. Blaikley, Carol Walker, Lydia Hulme, Eric Bernhard, Sandra Codlin, Jürg Bähler, Robin Allshire, Simon Whitehall and Timothy C. Humphrey ()
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Chen-Chun Pai: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Rachel S. Deegan: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Lakxmi Subramanian: Wellcome Trust Centre for Cell Biology, Institute of Cell Biology, The University of Edinburgh
Csenge Gal: Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University
Sovan Sarkar: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Elizabeth J. Blaikley: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Carol Walker: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Lydia Hulme: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Eric Bernhard: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford
Sandra Codlin: University College London, Evolution and Environment
Jürg Bähler: University College London, Evolution and Environment
Robin Allshire: Wellcome Trust Centre for Cell Biology, Institute of Cell Biology, The University of Edinburgh
Simon Whitehall: Institute for Cell and Molecular Biosciences, The Medical School, Newcastle University
Timothy C. Humphrey: CRUK MRC Oxford Institute for Radiation Oncology, University of Oxford

Nature Communications, 2014, vol. 5, issue 1, 1-11

Abstract: Abstract DNA double-strand break (DSB) repair is a highly regulated process performed predominantly by non-homologous end joining (NHEJ) or homologous recombination (HR) pathways. How these pathways are coordinated in the context of chromatin is unclear. Here we uncover a role for histone H3K36 modification in regulating DSB repair pathway choice in fission yeast. We find Set2-dependent H3K36 methylation reduces chromatin accessibility, reduces resection and promotes NHEJ, while antagonistic Gcn5-dependent H3K36 acetylation increases chromatin accessibility, increases resection and promotes HR. Accordingly, loss of Set2 increases H3K36Ac, chromatin accessibility and resection, while Gcn5 loss results in the opposite phenotypes following DSB induction. Further, H3K36 modification is cell cycle regulated with Set2-dependent H3K36 methylation peaking in G1 when NHEJ occurs, while Gcn5-dependent H3K36 acetylation peaks in S/G2 when HR prevails. These findings support an H3K36 chromatin switch in regulating DSB repair pathway choice.

Date: 2014
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DOI: 10.1038/ncomms5091

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