Abstract
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.
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