UMass Chan Medical School Faculty Publications


Nucleosome dynamics as modular systems that integrate DNA damage and repair

UMMS Affiliation

Program in Molecular Medicine

Publication Date


Document Type



Chromatin; *DNA Breaks, Double-Stranded; DNA Repair; Histones; *Models, Genetic; Nucleosomes


Molecular Biology


By some estimates, a eukaryotic cell must repair up to 10,000 DNA lesions per cell cycle to counteract endogenous sources of DNA damage. Exposure to environmental toxins, UV sources, or other radiations only increases this enormous number. Failure to repair such lesions can lead to a deleterious mutation rate, genomic instability, or cell death. The timely and efficient repair of eukaryotic DNA damage is further complicated by the realization that DNA lesions must be detected and repaired in the context of chromatin with its complex organization within the nucleus. Numerous studies have shown that chromatin packaging can inhibit nearly all repair pathways, and recent work has defined specific mechanisms that facilitate DNA repair within the chromatin context. In this review, we provide a broad overview of chromatin regulatory mechanisms, mainly at the nucleosomal level, and then focus on recent work that elucidates the role of chromatin structure in regulating the timely and efficient repair of DNA double-strand breaks (DSBs).

DOI of Published Version



Cold Spring Harb Perspect Biol. 2013 Sep 1;5(9). pii: a012658. doi: 10.1101/cshperspect.a012658. Link to article on publisher's site

Related Resources

Link to Article in PubMed

Journal/Book/Conference Title

Cold Spring Harbor perspectives in biology

PubMed ID