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Philos Trans R Soc Lond B Biol Sci. 2017 Oct 5;372(1731). pii: 20160281. doi: 10.1098/rstb.2016.0281.

SUMO, a small, but powerful, regulator of double-strand break repair.

Author information

1
Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences, Medical and Dental School, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
2
Birmingham Centre for Genome Biology and Institute of Cancer and Genomic Sciences, Medical and Dental School, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK j.morris.3@bham.ac.uk.

Abstract

The response to a DNA double-stranded break in mammalian cells is a process of sensing and signalling the lesion. It results in halting the cell cycle and local transcription and in the mediation of the DNA repair process itself. The response is launched through a series of post-translational modification signalling events coordinated by phosphorylation and ubiquitination. More recently modifications of proteins by Small Ubiquitin-like MOdifier (SUMO) isoforms have also been found to be key to coordination of the response (Morris et al. 2009 Nature462, 886-890 (doi:10.1038/nature08593); Galanty et al. 2009 Nature462, 935-939 (doi:10.1038/nature08657)). However our understanding of the role of SUMOylation is slight compared with our growing knowledge of how ubiquitin drives signal amplification and key chromatin interactions. In this review we consider our current knowledge of how SUMO isoforms, SUMO conjugation machinery, SUMO proteases and SUMO-interacting proteins contribute to directing altered chromatin states and to repair-protein kinetics at a double-stranded DNA lesion in mammalian cells. We also consider the gaps in our understanding.This article is part of the themed issue 'Chromatin modifiers and remodellers in DNA repair and signalling'.

KEYWORDS:

SUMO; SUMO protease; double-strand break repair; ubiquitin

PMID:
28847818
PMCID:
PMC5577459
DOI:
10.1098/rstb.2016.0281
[Indexed for MEDLINE]
Free PMC Article

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