Rsf- mutants of Escherichia coli HfrC defective in the production of the factor stimulating recombination in conjugation
1974
Male strains of Escherichia coli K12 excrete a protein which stimulates recombination in conjugation. The properties of four Rsf- mutants unable to produce this recombination-stimulating factor (RSF) have been studied. Two of the mutants have a pleiotropic phenotype which includes hypersensitivity to the lethal effects of ultraviolet (UV) and monofunctional alkylating agents (MAA) and markedly decreased growth rates at elevated temperatures. The latter property is associated with a diminished rate of DNA synthesis. Many more single-strand breaks are detected in the DNA of the pleiotropic mutants after MAA treatment than in the wild type, which are, however, repaired during incubation of the Rsf- cells after the treatment. No changes in UV-induced DNA breakdown or in host-cell reactivation of bacteriophage T1 have been detected in the mutant. The complete restoration of the wild type characters in Rsf+ revertants of these mutants proves that their complex phenotype is due to a single pleiotropic mutation. The integration of the wild type F factor into the chromosome of a derivative of a pleiotropic mutant retaining a portion of a previously integrated sex factor results in the complete restoration of the wild phenotype, which implies that the Rsf- mutation is located in the episomal DNA. These results show that some products specified by the F factor are necessary for the maintaince of the wild phenotype of Hfr cells. Possible mechanisms of this phenomenon are discussed.
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