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Transduction of R Factors with Phage P1 from Recombination‐Deficient Escherichia coli
Author(s) -
Hashimoto Hajime,
Iyobe Shizuko,
Mitsuhashi Susumu
Publication year - 1970
Publication title -
japanese journal of microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0021-5139
DOI - 10.1111/j.1348-0421.1970.tb00539.x
Subject(s) - transduction (biophysics) , dna , recombination , biology , genome , genetics , phagemid , microbiology and biotechnology , lysogenic cycle , escherichia coli , bacteriophage , gene , biochemistry
In the transduction of R factor with phage P1 from rec − host, transduction frequency was less than that from the rec + host but no segregation of resistance markers took place. However, a low percent of segregation was found in the transduction from rec + host. In contrast, phage particles of small size contained in P1 lysate could not transduce R factor even from a rec + host, although they could transduce chromosomal markers as did the usual P1 lysate. Recombination of the R factor took place in the rec − host at a frequency similar to the rec − host. Considering from the results that P1 is capable of transducing a DNA fragment of the same size as that of phage P1, it was concluded that the molecular weight of R factor DNA is smaller than that of phage P1 (6×10 7 daltons) but larger than that of small P1 particle (2.4×10 7 daltons). When transduced with phage P1, the R factor genome has to become a DNA fragment of the same size as the P1 particle by addition of other DNA following the recombination between R factor and Pl in rec + host. Hence, the segregation of markers of the R factor takes place on occasion by this recombination. From the assumption that phage Pl cannot recombine with the R factor in rec − host, it was predicted that the R factor genome becomes a DNA fragment of large enough size for transduction with P1 by polymerization of the R genome itself. This possibly could explain the decrease in transduction frequency from a rec − host and no segregation of the resistance markers of R factor in transduction from rec − host.