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Nucleic Acids Research Advance Access published online on May 28, 2008
Nucleic Acids Research, doi:10.1093/nar/gkn311
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

A single amino acid change in histone H4 enhances UV survival and DNA repair in yeast

Ronita Nag, Feng Gong, Deirdre Fahy and Michael J. Smerdon*

Biochemistry and Biophysics, School of Molecular Biosciences,Washington State University, Pullman, WA 99164-4660

*To whom correspondence should be addressed. Tel: +1 509 335 6853; Fax: +1 509 335 9688; Email: smerdon{at}wsu.edu

Received March 19, 2008. Revised April 27, 2008. Accepted April 29, 2008.

Single amino acid changes at specific DNA contacts of histones H3 and H4 generate SWI/SNF-independent (Sin) mutants in yeast. We have analyzed the effect of the Sin mutation at R45 of histone H4 on cell survival following UV irradiation, nucleotide excision repair (NER) and chromatin structure. We find that this mutation renders yeast cells more resistant to UV damage and enhances NER at specific chromatin loci. In the transcriptionally silent HML, repressed GAL10 and the constitutively active RPB2 loci, H4 R45 mutants exhibit enhanced repair of UV-induced cyclobutane pyrimidine dimers (CPDs) compared to wild-type (wt). However, the H4 R45 mutation does not increase the transcription of NER genes, disrupt transcriptional silencing of the HML locus or alter repression in the GAL10 locus. We have further shown that the H4 R45C mutation increases the accessibility of nucleosome DNA in chromatin to exogenous nucleases and may expedite nucleosome rearrangements during NER. Taken together, our results indicate that the increased repair observed in Sin mutants is a direct effect of the altered chromatin landscape caused by the mutation, suggesting that such subtle changes in the conserved histone residues can influence the accessibility of DNA repair factors in chromatin.

Present address: Feng Gong, Department of Biochemistry and Molecular Biology, School of Medicine, University of Miami, Coral Gables, FL-33124, USA Deirdre Fahy, Institute of Biological Chemistry, Washington State University, Pullman, WA 99164-6340, USA


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S. Chaudhuri, J. J. Wyrick, and M. J. Smerdon
Histone H3 Lys79 methylation is required for efficient nucleotide excision repair in a silenced locus of Saccharomyces cerevisiae
Nucleic Acids Res., April 1, 2009; 37(5): 1690 - 1700.
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