HIROTA Y, NISHIMURA Y, ORSKOV F, ORSKOV I
J Bacteriol. 1964 Feb;87(2):341-51. doi: 10.1128/jb.87.2.341-351.1964.
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.
广田幸典(日本大阪大学,大阪)、西村幸信、弗里茨·厄斯科夫和艾达·厄斯科夫。耐药因子R对大肠杆菌F特性的影响。《细菌学杂志》87:341 - 351。1964年。——用耐药因子R感染大肠杆菌雄性细胞(高频重组菌或F(+))会导致F因子的几种不同功能受到协同抑制:通过接合转移染色体的交配能力、f(+)抗原的产生以及雄性特异性噬菌体f1和核糖核酸噬菌体受体的形成。从野生型R因子(R(100))中分离出的R因子的i(-)突变体(R(100 - 1))对这些F特性没有抑制作用。雄性R(+)(100 - 1)细胞可自动凝集,但f(+)抗原仍然存在。当被R感染的雌性细胞获得了与F(-)菌株形成重组体的能力时,它们也变得可自动凝集。这些菌株中f(+)抗原是否存在的问题尚未解决。自动凝集的原因尚不清楚,但不是O抗原丧失的结果(粗糙型自动凝集)。对仅能在雌性细胞上形成噬菌斑的噬菌体tau的敏感性不受R因子存在与否的影响。在高频重组菌R(-)×F(-)和高频重组菌R(+)×F(-)的杂交中,未观察到重组体分离模式的差异。这些结果表明,R因子控制着由F因子在细胞表面形成的“F物质”合成中的关键机制。