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Review
. 2011 Sep 16;585(18):2914-9.
doi: 10.1016/j.febslet.2011.05.056. Epub 2011 Jun 12.

The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks

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Free article
Review

The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks

Simon Bekker-Jensen et al. FEBS Lett. .
Free article

Abstract

DNA double-strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non-proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB-modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin-dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin- and SUMO-dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair.

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