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We previously constructed an assay system for studying enterobacterial \u03b2-lactam resistance mutations using the well-developed genetics of\n                    <jats:italic>E. coli<\/jats:italic>\n                    by integrating enterobacterial\n                    <jats:italic>ampRC<\/jats:italic>\n                    genes into the\n                    <jats:italic>E. coli<\/jats:italic>\n                    chromosome. Like the cells of other enterobacteria,\n                    <jats:italic>E. coli<\/jats:italic>\n                    cells acquire \u03b2-lactam resistance by\n                    <jats:italic>ampD<\/jats:italic>\n                    mutation. Here we show that starvation and stress responses provoke\n                    <jats:italic>ampD<\/jats:italic>\n                    \u03b2-lactam resistance mutagenesis. When starved on lactose medium, Lac\n                    <jats:sup>\u2212<\/jats:sup>\n                    strains used in mutagenesis studies accumulate\n                    <jats:italic>ampD<\/jats:italic>\n                    \u03b2-lactam resistance mutations independent of Lac reversion. DNA double-strand break repair (DSBR) proteins and the SOS and RpoS stress responses are required for this mutagenesis, in agreement with the results obtained for\n                    <jats:italic>lac<\/jats:italic>\n                    reversion in these cells. Surprisingly, the stress-induced\n                    <jats:italic>ampD<\/jats:italic>\n                    mutations require DinB (DNA polymerase IV) and partially require error-prone DNA polymerase V, unlike\n                    <jats:italic>lac<\/jats:italic>\n                    mutagenesis, which requires only DinB. This assay demonstrates that real-world stressors, such as starvation, can induce clinically relevant resistance mutations. Finally, we used the\n                    <jats:italic>ampD<\/jats:italic>\n                    system to observe the true forward-mutation sequence spectrum of DSBR-associated stress-induced mutagenesis, for which previously only frameshift reversions were studied. We found that base substitutions outnumber frameshift mutations, as seen in other experimental systems showing stress-induced mutagenesis. The important evolutionary implication is that not only loss-of-function mutations but also change-of-function mutations can be generated by this mechanism.\n                  <\/jats:p>","DOI":"10.1128\/jb.00732-09","type":"journal-article","created":{"date-parts":[[2009,7,31]],"date-time":"2009-07-31T21:10:02Z","timestamp":1249074602000},"page":"5881-5889","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":85,"title":["Stress-Induced \u03b2-Lactam Antibiotic Resistance Mutation and Sequences of Stationary-Phase Mutations in the\n                    <i>Escherichia coli<\/i>\n                    Chromosome"],"prefix":"10.1128","volume":"191","author":[{"given":"Joseph F.","family":"Petrosino","sequence":"first","affiliation":[{"name":"Departments of Molecular and Human Genetics"},{"name":"Molecular Virology and Microbiology"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodrigo S.","family":"Galhardo","sequence":"additional","affiliation":[{"name":"Departments of Molecular and Human Genetics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liza D.","family":"Morales","sequence":"additional","affiliation":[{"name":"Departments of Molecular and Human Genetics"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Susan M.","family":"Rosenberg","sequence":"additional","affiliation":[{"name":"Departments of Molecular and Human Genetics"},{"name":"Molecular Virology and Microbiology"},{"name":"Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030-3411"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"2857","DOI":"10.1099\/00221287-145-10-2857","volume":"145","year":"1999","unstructured":"Alonso, A., E. 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