Abstract
We have recently demonstrated that Schizosaccharomyces pombe cells treated with the nucleoside analogue 5-azacytidine (5-azaC) require previously characterised G2 checkpoint mechanisms for survival. Here we present a survey of known DNA repair mutations which defines those genes required for survival in the presence of 5-azaC. Using a combination of single-mutant and epistasis analyses we find that the excision, mismatch and recombinational repair pathways are all required in some degree for the repair of 5-azaC-mediated DNA damage. There are distinct differences in the epistatic interactions of several of the repair mutations with respect to 5-azaC-mediated DNA damage relative to UV-mediated DNA damage.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphatases*
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Azacitidine / toxicity*
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Bacterial Proteins / genetics
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DNA Damage*
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DNA Repair*
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DNA-Binding Proteins / drug effects
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DNA-Binding Proteins / genetics
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Drug Resistance, Microbial / genetics
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Endodeoxyribonucleases*
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Escherichia coli Proteins*
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Fungal Proteins / drug effects
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Fungal Proteins / genetics
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MutS DNA Mismatch-Binding Protein
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Mutation
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Nucleotides / genetics
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Rad51 Recombinase
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Radiation Tolerance / genetics
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Recombination, Genetic
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Saccharomyces cerevisiae Proteins*
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Schizosaccharomyces / drug effects
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Schizosaccharomyces / genetics*
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Schizosaccharomyces pombe Proteins*
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Sequence Homology, Nucleic Acid
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Transcription Factors*
Substances
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Bacterial Proteins
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DNA-Binding Proteins
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Escherichia coli Proteins
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Fungal Proteins
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Nucleotides
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RAD18 protein, S cerevisiae
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RHP51 protein, S pombe
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Rad12 protein, Coprinus cinereus
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SWI4 protein, S cerevisiae
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Saccharomyces cerevisiae Proteins
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Schizosaccharomyces pombe Proteins
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Transcription Factors
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RAD2 protein, S cerevisiae
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Rad51 Recombinase
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Endodeoxyribonucleases
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Adenosine Triphosphatases
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MutS DNA Mismatch-Binding Protein
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MutS protein, E coli
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Azacitidine