Chromatin remodelling complex RSC promotes base excision repair in chromatin of Saccharomyces cerevisiae

Wioletta Czaja; Peng Mao; Michael J Smerdon

doi:10.1016/j.dnarep.2014.01.002

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Chromatin remodelling complex RSC promotes base excision repair in chromatin of Saccharomyces cerevisiae

Journal article

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Chromatin remodelling complex RSC promotes base excision repair in chromatin of Saccharomyces cerevisiae

Wioletta Czaja, Peng Mao and Michael J Smerdon

DNA repair, Vol.16(1), pp.35-43

04/2014

DOI: https://doi.org/10.1016/j.dnarep.2014.01.002

Handle:

https://hdl.handle.net/2376/106778

PMCID: PMC4026264

PMID: 24674626

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Abstract

Chromatin - metabolism

DNA, Fungal - genetics

Saccharomyces cerevisiae - genetics

Alkylating Agents - pharmacology

Saccharomyces cerevisiae - drug effects

Galactokinase - genetics

Gene Knockdown Techniques

DNA-Binding Proteins - metabolism

Saccharomyces cerevisiae - metabolism

DNA Methylation

Genome, Fungal

Cell Cycle Proteins - genetics

Nuclear Proteins - genetics

DNA Repair - drug effects

Cell Cycle Proteins - metabolism

Chromatin Assembly and Disassembly

Nuclear Proteins - metabolism

Saccharomyces cerevisiae Proteins - genetics

Transcription Factors - genetics

DNA-Binding Proteins - genetics

Transcription Factors - metabolism

Galactokinase - metabolism

Saccharomyces cerevisiae Proteins - metabolism

Chromatin - genetics

Methyl Methanesulfonate - pharmacology

The base excision repair (BER) pathway is a conserved DNA repair system required to maintain genomic integrity and prevent mutagenesis in all eukaryotic cells. Nevertheless, how BER operates in vivo (i.e. in the context of chromatin) is poorly understood. We have investigated the role of an essential ATP-dependent chromatin remodelling (ACR) complex RSC (Remodels the Structure of Chromatin) in BER of intact yeast cells. We show that depletion of STH1, the ATPase subunit of RSC, causes enhanced sensitivity to the DNA alkylating agent methyl methanesulfonate (MMS) and results in a substantial inhibition of BER, at the GAL1 locus and in the genome overall. Consistent with this observation, the DNA in chromatin is less accessible to micrococcal nuclease digestion in the absence of RSC. Quantitative PCR results indicate that repair deficiency in STH1 depleted cells is not due to changes in the expression of BER genes. Collectively, our data indicates the RSC complex promotes efficient BER in chromatin. These results provide, for the first time, a link between ATP-dependent chromatin remodelling and BER in living cells.

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Title: Chromatin remodelling complex RSC promotes base excision repair in chromatin of Saccharomyces cerevisiae
Creators: Wioletta Czaja - Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-7520, USA
Peng Mao - Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-7520, USA
Michael J Smerdon - Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-7520, USA. Electronic address: smerdon@wsu.edu
Publication Details: DNA repair, Vol.16(1), pp.35-43
Academic Unit: Molecular Biosciences, School of
Publisher: Netherlands
Grant note: R37 ES002614 / NIEHS NIH HHS R01 ES002614 / NIEHS NIH HHS ES002614 / NIEHS NIH HHS
Identifiers: 99900546702601842
Language: English
Resource Type: Journal article