Non-random distribution of transduction termini in transductants from the integrated R plasmid, R100-1 |
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Authors: | Hirofumi Danbara and Masanosuke Yoshikawa |
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Affiliation: | (1) The Institute of Medical Science, The University of Tokyo, Minato-ku, Shiroganedai 4-6-1, Tokyo, Japan;(2) Present address: Max-Planck Institut für Molekulare Genetik, Ihnestraße 63-73, D-1000 Berlin 33 |
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Abstract: | Summary Tra+and tra–derivatives of drug resistance plasmid, R100-1, were isolated by phage P1 from an Hfr donor with integrated R100-1 and then analyzed by complementation tests with tra–point mutants of Flac. Tra+derivatives of R100-1 carrying tetracycline resistance alone and those carrying all six drug-resistance genes could support transfer of tra–point mutants of Flac except Flac traJ, whereas all of tra–derivatives of R100-1 failed to complement any one of tra–point mutants of Flac. This suggests that these tra–derivatives of R100-1 carrying tetracycline resistance gene are deleted for all the transfer genes impaired in the Flac point mutants tested. We assume a hot point , probably a specific base sequence similar to an IS element, at the left of the tetracycline gene (Fig. 1) becomes a transduction terminus in transduction of the integrated R100-1 by phage P1. Complementation analysis of tra–derivatives carrying five resistance genes except the tetracycline gene led us to a supposition that a gene(s), probably analogous to traJ of the F plasmid, is located on R100-1 near the tetracycline gene which plays an important regulatory role for self-transfer as well as for the complementation of tra–Flac mutants. |
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