A new class of mutations altering the response of the ribosome to streptomycin.
Mutants were isolated from high-level streptomycin dependent strains of Escherichia coli B, which do not spontaneously revert to antibiotic independence. In these mutants the requirement for streptomycin was much reduced, but not abolished. The relieving of the antibiotic dependence was caused by qui (for quasi-independent) mutations. These were analogous to the ramA (rpsD) mutations which relieve the streptomycin requirement of other classes of streptomycin dependent mutants, but strains harboring qui mutations exhibited novel streptomycin phenotypes in conjunction with all rpsL (strA) alleles. RamA mutations increase ribosomal misreading; qui mutations either did not significantly alter misreading, or else reduced it.
D003090:Coliphages / Q000235:genetics; D003227:Conjugation, Genetic; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000235:genetics* / Q000302:isolation & purification; D029968:Escherichia coli Proteins; D009154:Mutation; D010641:Phenotype; D014176:Protein Biosynthesis; D000091243:Ribosomal Protein S9; D012270:Ribosomes / Q000378:metabolism*; D013307:Streptomycin / Q000494:pharmacology*; D014161:Transduction, Genetic
D029968:Escherichia coli Proteins; D000091243:Ribosomal Protein S9; C000717190:RpsI protein, E coli; D013307:Streptomycin