Derepression of F factor function in Salmonella typhimurium

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Abstract
In S. typhimurium LT2 the F factor of Escherichia coli K-12 replicates normally but is repressed; Flac+ cells give no visible lysis on solid media with male-specific phages, low frequency transfer of Flac+ (0.001-0.007/donor cell), few f2 infective centers (0.002-0.006/cell) and they propagate male-specific phages to low titers; they display a Fin+ (fertility inhibition) phenotype. This repression, owing to pSLT, a 60 Mdal [megadalton] plasmid normally resident in S. typhimurium, was circumvented by the following materials: Flac+ plasmids from E. coli with mutations in finP or traO; S. typhimurium line which was cured of pSLT; pKZl, a KmR plasmid in the same Inc group as pSLT, which caused expulsion of pSLT and made Fin- lines; F-Fin- mutants which originated spontaneously and which are present in most Hfr strains of S. typhimurium. Strains which are derepressed for F function by the above methods give visible lysis on solid media with male-specific phages, .apprx. 1.0 Lac+ recombinants/donor cell in conjugal transfer, .apprx. 0.82 f2 infective centers/cell, over 80% of cells with visible F pili, and propagation of male-specific phages to high titer. These data confirm earlier observations that pSLT represses F by the FinOP system. There is no other mechanism which represses F function in S. typhimurium. If donor function is derepressed by one of the above methods and if rough recipient strains are used, F-mediated conjugation in S. typhimurium LT2 is as efficient as in E. coli K-12.

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