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pubmed:abstractText |
Hirota, Yukinori (Osaka University, Osaka, Japan), Yukinobu Nishimura, Frits Ørskov, and Ida Ørskov. Effect of drug-resistance factor R on the F properties of Escherichia coli. J. Bacteriol. 87:341-351. 1964.-Infection of Escherichia coli male cells (Hfr or F(+)) with resistance factor R results in the co-ordinate inhibition of several distinct functions of F factor: mating capacity to transfer chromosome by conjugation, production of f(+) antigen, and formation of receptors for the male-specific bacteriophages, f1 and ribonucleic acid phage. The i(-) mutant (R(100-1)) of R factor, which was isolated from wild-type R factor (R(100)), shows no inhibition of these F properties. Male R(+) (100-1) cells were autoagglutinable but the f(+) antigen was still present. When R-infected female cells had acquired the ability to form recombinants with an F(-) strain, they also had become autoagglutinable. The question of the presence of f(+) antigen in these strains was not solved. The cause of the autoagglutinability is not known, but it is not the result of loss of O antigen (rough autoagglutinability). Sensitivity to a phage tau, which can form plaques on female cells only, is not affected by the presence or absence of R factor. No difference in the pattern of segregation of recombinants was observed between the cross of Hfr R(-) x F(-) and that of Hfr R(+) x F(-). These results indicate that R factor controls a key mechanism in the synthesis of "F substances" formed on the cell surface by the F factor.
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