Skip to main content
Genetics logoLink to Genetics
. 1976 Jul;83(3):459–475.

Specialized Transducing Phages Derived from Phage P22 That Carry the proAB Region of the Host, SALMONELLA TYPHIMURIUM: Genetic Evidence for Their Structure and Mode of Transduction

Adrienne P Jessop 1
PMCID: PMC1213526  PMID: 783005

Abstract

Two independently isolated specialized transducing phages, P22 pro-1 and P22pro-3, have been studied. Lysates of P22pro-1 contain a majority of transducing phages which can go through the lytic cycle only in mixed infection; these defective phages transduce by lysogenization in mixed infection and by substitution in single infection. A few of the transducing phages in P22pro-1 lysates appear to be non-defective, being able to form plaques and to transduce by lysogenization in single infection. Transduction by P22pro-3 lysates is effected by non-defective transducing phages, which transduce by lysogenization; these lysates also contain a majority of defective phages which do not co-operate in mixed infection.

The P22 pro-1 genome is thought to contain an insertion of bacterial DNA longer than the terminal repetition present in P22 wild type, so that at maturation a population of differently defective phages is produced. The exact structure of the P22pro-3 genome is open to conjecture, but it seems clear that the insertion of bacterial DNA is smaller than that in P22pro-1. Both P22pro-1 and P22pro-3 are defective in integration at ataA under non-selective conditions, although both integrate on medium that lacks proline.

Full Text

The Full Text of this article is available as a PDF (1.1 MB).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Botstein D., Matz M. J. A recombination function essential to the growth of bacteriophage P22. J Mol Biol. 1970 Dec 28;54(3):417–440. doi: 10.1016/0022-2836(70)90119-1. [DOI] [PubMed] [Google Scholar]
  2. Botstein D. Synthesis and maturation of phage P22 DNA. I. Identification of intermediates. J Mol Biol. 1968 Jun 28;34(3):621–641. doi: 10.1016/0022-2836(68)90185-x. [DOI] [PubMed] [Google Scholar]
  3. Chan R. K., Botstein D. Genetics of bacteriophage P22. I. Isolation of prophage deletions which affect immunity to superinfection. Virology. 1972 Jul;49(1):257–267. doi: 10.1016/s0042-6822(72)80027-8. [DOI] [PubMed] [Google Scholar]
  4. Smith-Keary P. F. Restricted trandsuction by bacteriophage P22 in Salmonella typhimurium. Genet Res. 1966 Aug;8(1):73–82. doi: 10.1017/s0016672300009927. [DOI] [PubMed] [Google Scholar]
  5. Smith H. O. Defective phage formation by lysogens of integration deficient phage P22 mutants. Virology. 1968 Feb;34(2):203–223. doi: 10.1016/0042-6822(68)90231-6. [DOI] [PubMed] [Google Scholar]
  6. Smith H. O., Levine M. A phage P22 gene controlling integration of prophage. Virology. 1967 Feb;31(2):207–216. doi: 10.1016/0042-6822(67)90164-x. [DOI] [PubMed] [Google Scholar]
  7. Tye B. K., Chan R. K., Botstein D. Packaging of an oversize transducing genome by Salmonella phage P22. J Mol Biol. 1974 Jan 5;85(4):485–500. doi: 10.1016/0022-2836(74)90311-8. [DOI] [PubMed] [Google Scholar]
  8. Watanabe T., Ogata Y., Chan R. K., Botstein D. Specialized transduction of tetracycline resistance by phage P22 in Salmonella typhimurium. I. Transduction of R factor 222 by phage P22. Virology. 1972 Dec;50(3):874–882. doi: 10.1016/0042-6822(72)90441-2. [DOI] [PubMed] [Google Scholar]

Articles from Genetics are provided here courtesy of Oxford University Press

RESOURCES