Suppression of mutations conferring penicillin tolerance by interference with the stringent control mechanism of Escherichia coli.
Mutations in Escherichia coli previously reported (R. E. Harkness and E. E. Ishiguro, J. Bacteriol. 155:15-21, 1983; L. C. Shimmin, D. Vanderwel, R. E. Harkness, B. R. Currie, A. Galloway, and E. E. Ishiguro, J. Gen. Microbiol. 130:1315-1323, 1984) as conferring a temperature-dependent tolerance to lysis induced by inhibitors of peptidoglycan synthesis were suppressed by treatment with inhibitors of the stringent response or by introduction of a relA mutation. The relA+ derivatives of the mutants exhibited a stringent response at the nonpermissive temperature. The consequent inhibition of the autolytic enzyme system (W. Kusser and E. E. Ishiguro, J. Bacteriol. 164:861-865, 1985) was apparently responsible for the lysis-tolerant phenotypes of these mutants.
Kusser
W
W
Ishiguro
E E
EE
D000667:Ampicillin / Q000494:pharmacology*; D001433:Bacteriolysis / Q000187:drug effects; D002701:Chloramphenicol / Q000494:pharmacology; D004361:Drug Tolerance; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D005839:Gentamicins / Q000494:pharmacology; D007612:Kanamycin / Q000494:pharmacology; D010641:Phenotype; D013489:Suppression, Genetic; D013696:Temperature
D005839:Gentamicins; D007612:Kanamycin; D002701:Chloramphenicol; D000667:Ampicillin