Genetic and phenotypic identification of XXXX -resistant mutants with the small-colony-variant phenotype in @entity794 .

@entity1 @entity6723 @entity8197 @entity12119 @entity535 @entity794 @entity581
Small-colony variants (SCVs) of @entity794 are a slow-growing subpopulation whose phenotypes can include resistance to @entity581 , defects in electron transport, and enhanced persistence in @entity1 cells. Here we show that a subset of mutants selected as SCVs by reduced susceptibility to @entity581 are resistant to the antibiotic @entity12119 (FA) and conversely that a subset of mutants selected for resistance to FA are SCVs. Mutation analysis reveals different genetic classes of FA-resistant SCVs. One class, FusA-SCVs, have @entity535 substitution mutations in the ribosomal translocase EF-G different from those found in classic FusA mutants. Most of these mutations are located in structural domain V of EF-G, but some are in domain I or III. FusA-SCVs are auxotrophic for hemin. A second class of FA-resistant SCVs carry mutations in rplF, coding for ribosomal protein L6, and are designated as FusE mutants. FusE mutants fall into two phenotypic groups: one auxotrophic for hemin and the other auxotrophic for @entity8197 . Accordingly, we have identified new genetic and phenotypic classes of FA-resistant mutants and clarified the genetic basis of a subset of @entity794 @entity6723 mutants. A clinical implication of these data is that FA resistance could be selected by antimicrobial agents other than FA.
