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- Robert B. Helling
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Brian K. Janes
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Heather Kimball
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Timothy Tran
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Michael Bundesmann
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Pietra Check
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Darcy Phelan
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
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- Charles Miller
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109-1048
説明
<jats:title>ABSTRACT</jats:title> <jats:p> About 10% of the nalidixic acid-resistant (Nal <jats:sup>r</jats:sup> ) mutants in a transposition-induced library exhibited a growth factor requirement as the result of <jats:italic>cysH</jats:italic> , <jats:italic>icdA</jats:italic> , <jats:italic>metE</jats:italic> , or <jats:italic>purB</jats:italic> mutation. Resistance in all of these mutants required a functional AcrAB-TolC efflux pump, but the EmrAB-TolC pump played no obvious role. Transcription of <jats:italic>acrAB</jats:italic> was increased in each type of Nal <jats:sup>r</jats:sup> mutant. In the <jats:italic>icdA</jats:italic> and <jats:italic>purB</jats:italic> mutants, each of the known signaling pathways appeared to be used in activating the AcrAB-TolC pump. The metabolites that accumulate upstream of the blocks caused by the mutations are hypothesized to increase the levels of the AcrAB-TolC pump, thereby removing nalidixic acid from the organism. </jats:p>
収録刊行物
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- Journal of Bacteriology
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Journal of Bacteriology 184 (13), 3699-3703, 2002-07
American Society for Microbiology