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Inactivation of mutS Leads to a Multiple-Drug Resistance in Pseudomonas putida ATCC12633  

KIM JEONG-NAM (Department of Biology, Research Institute for Basic Science, Kyung Hee University)
LEE SUNG-JAE (Department of Biology, Research Institute for Basic Science, Kyung Hee University)
LEE HO-SA (Department of Biology, Research Institute for Basic Science, Kyung Hee University)
RHIE HO-GUN (Department of Biology, Research Institute for Basic Science, Kyung Hee University)
Publication Information
Journal of Microbiology and Biotechnology / v.15, no.6, 2005 , pp. 1214-1220 More about this Journal
Abstract
Decreased porin-mediated outer membrane penetration of hydrophilic antibiotics is a common mechanism of antibiotic resistance in Gram-negative bacteria. This study was undertaken to determine whether a null mutation in Pseudomonas putida would suppress porin synthesis, and therefore reduce the susceptibility of the organism to streptomycin, norfloxacin, and tetracycline. Inverse PCR amplification and double-stranded DNA sequencing were used to identify chromosomal genes carrying TnphoA'-1 inserts. Genome database available was used to identify putative homologue genes, one of which encodes protein with homology to domains of the MutS of P. putida, suggesting a crucial role in the multidrug resistance. Increased resistance to streptomycin, norfloxacin, and tetracycline might be due to accumulation of compensatory mutations. Either no growth or slow growth was observed in P. putida KH1027 when grown in minimal medium containing gluconate, glucose, or citrate; however, it is not clear whether the growth patterns contributed to the multidrug resistance.
Keywords
Pseudomonas putida; inverse PCR; DNA sequencing; multidrug resistance;
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