Abstract
In vivo experiments with heteroduplex lambda genomes show that the MutY mismatch repair system of Escherichia coli defines an average repair tract that is shorter than 27 nucleotides and longer than 9 nucleotides and extends 3' from the corrected adenine. The phenotype of a mutant defective in DNA polymerase I shows that this enzyme plays a significant, though not an essential, role in the in vivo repair of apurinic sites generated by this system. Evidence is presented that in the absence of polymerase I the repair tracts are modestly longer than in the polA+ extending in the 5' direction from the corrected adenine, suggesting a role for another DNA polymerase.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphatases*
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Bacterial Proteins / genetics
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Bacteriophage lambda / genetics
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Colony Count, Microbial
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DNA Glycosylases*
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DNA Polymerase I / genetics
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DNA Polymerase I / metabolism*
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DNA Repair*
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DNA, Bacterial / metabolism*
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Escherichia coli / enzymology*
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Escherichia coli / genetics
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Escherichia coli / metabolism
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Escherichia coli Proteins*
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MutL Proteins
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Mutagenesis, Insertional
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N-Glycosyl Hydrolases / metabolism*
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Nucleic Acid Heteroduplexes
Substances
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Bacterial Proteins
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DNA, Bacterial
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Escherichia coli Proteins
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MutL protein, E coli
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Nucleic Acid Heteroduplexes
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DNA Polymerase I
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DNA Glycosylases
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N-Glycosyl Hydrolases
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mutY adenine glycosylase
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Adenosine Triphosphatases
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MutL Proteins