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Streptomycin- and rifampin-resistant mutants of Escherichia coli perturb F exclusion of bacteriophage T7 by affecting synthesis of the F plasmid protein PifA
Author(s) -
Christian Schmidt,
Priscilla Kemp,
Ian J. Molineux
Publication year - 1995
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.177.6.1589-1594.1995
Subject(s) - rpob , biology , operon , bacteriophage , streptomycin , plasmid , mutant , escherichia coli , microbiology and biotechnology , mutation , dna gyrase , genetics , lysogenic cycle , allele , repressor , dna , antibiotics , bacteria , gene , 16s ribosomal rna , transcription factor
Certain alleles of rpsL that confer resistance to the antibiotic streptomycin almost completely relieve F exclusion of bacteriophage T7. Introduction of a specific rpoB allele conferring resistance to rifampin into the rpsL strain restores the ability of the F-containing strain to exclude T7. This variation in the severity of F exclusion is reflected in the levels of the F-encoded inhibitor protein PifA: F'-containing cells that harbor specific rpsL alleles are phenotypically Pif-, but become Pif+ by the further acquisition of a specific rpoB allele. F-containing cells harboring the gyrA43(Ts) mutation also appear phenotypically Pif-, possibly because repression of the pif operon is enhanced by an altered DNA conformation in the gyrase mutant strain.

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