The nucleosome-binding protein HMGN2 modulates global genome repair
Authors: Subramanian, Mangalam1; Gonzalez, Rhiannon W.1; Patil, Hemangi1; Ueda, Takahiro; Lim, Jae-Hwan; Kraemer, Kenneth H.2; Bustin, Michael3; Bergel, Michael
Source: FEBS Journal, Volume 276, Number 22, November 2009 , pp. 6646-6657(12)
Publisher: Blackwell Publishing
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Abstract:
The HMGN family comprises nuclear proteins that bind to nucleosomes and alter the structure of chromatin. Here, we report that DT40 chicken cells lacking either HMGN2 or HMGN1a, or lacking both HMGN1a and HMGN2, are hypersensitive to killing by UV irradiation. Loss of both HMGN1a and HMGN2 or only HMGN2 increases the extent of UV-induced G2-M checkpoint arrest and the rate of apoptosis. HMGN null mutant cells showed slower removal of UV-induced DNA lesions from native chromatin, but the nucleotide excision repair remained intact, as measured by host cell reactivation assays. These results identify HMGN2 as a component of the global genome repair subpathway of the nucleotide excision repair pathway, and may indicate that HMGN2 facilitates the ability of the DNA repair proteins to access and repair UV-induced DNA lesions in chromatin. Our finding that HMGNs play a role in global DNA repair expands the role of these proteins in the maintenance of genome integrity.Keywords: apoptosis; cell cycle; chromatin; DNA repair; UV irradiation
Document Type: Research article
DOI: 10.1111/j.1742-4658.2009.07375.x
Affiliations: 1: Department of Biology, Texas Woman's University, Denton, TX, USA 2: Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA 3: Protein Section, Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA
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