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We show that\n            <jats:italic>moa<\/jats:italic>\n            mutants exposed to HAP also exhibit elevated mutagenesis, a hyperrecombination phenotype, and increased SOS induction. The\n            <jats:italic>E. coli rdgB<\/jats:italic>\n            gene encodes a protein homologous to a deoxyribonucleotide triphosphate pyrophosphatase from\n            <jats:italic>Methanococcus jannaschii<\/jats:italic>\n            that shows a preference for purine base analogs.\n            <jats:italic>moa rdgB<\/jats:italic>\n            mutants are extremely sensitive to killing by HAP and exhibit increased mutagenesis, recombination, and SOS induction upon HAP exposure. Disruption of the endonuclease V gene,\n            <jats:italic>nfi<\/jats:italic>\n            , rescues the HAP sensitivity displayed by\n            <jats:italic>moa<\/jats:italic>\n            and\n            <jats:italic>moa rdgB<\/jats:italic>\n            mutants and reduces the level of recombination and SOS induction, but it increases the level of mutagenesis. Our results suggest that endonuclease V incision of DNA containing HAP leads to increased recombination and SOS induction and even cell death. Double-strand break repair mutants display an increase in HAP sensitivity, which can be reversed by an\n            <jats:italic>nfi<\/jats:italic>\n            mutation. This suggests that cell killing may result from an increase in double-strand breaks generated when replication forks encounter endonuclease V-nicked DNA. We propose a pathway for the removal of HAP from purine pools, from deoxynucleotide triphosphate pools, and from DNA, and we suggest a general model for excluding purine base analogs from DNA. The system for HAP removal consists of a molybdoenzyme, thought to detoxify HAP, a deoxyribonucleotide triphosphate pyrophosphatase that removes noncanonical deoxyribonucleotide triphosphates from replication precursor pools, and an endonuclease that initiates the removal of HAP from DNA.\n          <\/jats:p>","DOI":"10.1128\/jb.185.10.3101-3110.2003","type":"journal-article","created":{"date-parts":[[2003,5,2]],"date-time":"2003-05-02T16:23:48Z","timestamp":1051892628000},"page":"3101-3110","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["Repair System for Noncanonical Purines in\n            <i>Escherichia coli<\/i>"],"prefix":"10.1128","volume":"185","author":[{"given":"Nicholas E.","family":"Burgis","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, The University at Albany, State University of New York, Albany, New York 12222"}]},{"given":"Jason J.","family":"Brucker","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, The University at Albany, State University of New York, Albany, New York 12222"}]},{"given":"Richard P.","family":"Cunningham","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, The University at Albany, State University of New York, Albany, New York 12222"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"12261","DOI":"10.1074\/jbc.275.16.12261","volume":"275","year":"2000","unstructured":"Arnold, D. 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