Watanabe T, Sakaizumi S, Furuse C
J Bacteriol. 1968 Nov;96(5):1796-802. doi: 10.1128/jb.96.5.1796-1802.1968.
Superinfection immunity is found in the conjugal transfer of R factors between two fi(+) R factors and between two fi(-) R factors (fi = fertility inhibition), as we reported previously. In contrast, no reduction in the frequencies of transduction of an fi(+) R factor 222 was caused by the presence of fi(+) R factors in the recipients in transduction systems with phage P1kc in Escherichia coli K-12 and with phage P22 in Salmonella typhimurium LT-2. The absence of superinfection immunity in transduction may be due to the difference in the route of entry of the R factor. The frequencies of transduction of an fi(+) R factor were reduced, although slightly, by the presence of fi(-) R factors in the recipients. This reduction is probably due to host-controlled restriction of the entering fi(+) R factor by the fi(-) R factors in the recipients, since transduction of an fi(+) R factor by the transducing phage propagated on the strain carrying both fi(+) and fi(-) R factors was not reduced by the presence of homologous fi(-) R factors in the recipients. The fi(+) R factor 222, when transduced to the recipient strains carrying other R factors, recombined genetically at high frequencies with these resident R factors, regardless of their fi type.
如我们之前所报道的,在两个fi(+) R因子之间以及两个fi(-) R因子之间(fi = 育性抑制)的R因子接合转移中发现了超感染免疫。相比之下,在大肠杆菌K-12中使用噬菌体P1kc以及在鼠伤寒沙门氏菌LT-2中使用噬菌体P22的转导系统中,受体中存在fi(+) R因子并不会导致fi(+) R因子222转导频率的降低。转导中缺乏超感染免疫可能是由于R因子进入途径的差异。受体中存在fi(-) R因子会使fi(+) R因子的转导频率降低,尽管降低幅度较小。这种降低可能是由于受体中的fi(-) R因子对进入的fi(+) R因子进行宿主控制的限制,因为在携带fi(+)和fi(-) R因子的菌株上繁殖的转导噬菌体对fi(+) R因子的转导不会因受体中同源fi(-) R因子的存在而降低。当fi(+) R因子222转导到携带其他R因子的受体菌株时,无论这些常驻R因子的fi类型如何,它都能与它们高频遗传重组。