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Impaired Transduction of R213 and Its Recovery by a Homologous Resident R Factor

^a Department of Biology, School of Science, University of Osaka, Osaka, Japan

ABSTRACT

Transduction by Plkc of drug-resistance markers of the factor R213 was shown to occur at an exceptionally low frequency (at less than 10^–8 of the input phage), and they could not be transduced by P22. When the recipient cells carried a homologous R factor derived from R213, markers were transduced by Plkc at a normal frequency (at about 10^–5 to 10^–6 of the input phage). Derivative R factors, transducible by Plkc at a normal frequency but being transferred by conjugation at a frequency lower than that of the original R213, were obtained. This type of transductant often segregated R^– cells. In addition, several transductants contained R factors which were transferred normally by conjugation but were transduced by Plkc at as low a frequency as the original R213. This type of transductant was an effective recipient for transduction by Plkc of R213 when apparently "cured" by acridine treatment. No such effective "cured" recipients were obtained from the transductants with derivatives of R213 transducible at a normal frequency. Two possible interpretations are presented: (i) R213 produces a bacteriocin-like substance upon transduction, or (ii) the genome size of R213 is too large for all of its determinants to be transduced.

¹ Present address: Department of Bacterial Infection, The Institute of Medical Science, The University of Tokyo, P.O. 108, Minato-ku, Tokyo, Japan.

² Present address: Institut Pasteur, 75 Paris, France.