Control of the Replication Complex of Bacteriophage P22

Self Cite

Infection of Salmonella typhimnurium with phage P22 causes a decrease in the activity of host deoxyribonuclease which degrades single-stranded deoxyribonucleic acid (DNA). This decrease is reversed when the infecting phage is P22c+; it is not-°o i reversed if the infecting phage kills the cell. The decrease does not occur in infections 4* with P22ts25.1 (which only adsorbs and injects DNA) or in infections of a lysogen by a nonvirulent phage. It does occur, however, after infections with other phages which are blocked in phage DNA synthesis. Inhibiting protein synthesis with chloramphenicol does not in itself cause the decrease in uninfected cells, but it does prevent infected cells from showing this effect.

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Inhibitory Effect of Bacteriophage P22 Infection on Host Cell Deoxyribonuclease Activity

Israel

Woodworth-Gutai

Levine

1972

Self Cite

“…It should be possible to separate the early activities required for viable phage production from those that occur late in I Present addres: Virology Section, The Weizmann Institute of Science, Rehovot, Israel. infection (assembly). Temperature-sensitive mutants for gene 16 have been found and are described in this paper. P22 16-ts phages conform to the expected phenotype for mutant phage containing thermolabile P16 in the virion.…”

mentioning

confidence: 92%

“…We have characterized a mutant of P22 carrying a temperature-sensitive allele of gene 16. This mutant has previously been referred to as P2225-ts (Levine et al, 1970(Levine et al, , 1972 and P22 X-ts Soska, 1970, 1973). P22 16-ts behaves as an early mutant at the nonpermissive temperature.…”

mentioning

confidence: 99%

Bacteriophage P22 virion protein which performs an essential early function. I. Analysis of 16-ts mutants

Hoffman¹,

Levine²

1975

The product of gene 16 of phage P22, P16, is a head protein. P16 does not play an essential role in phage assembly since particles formed without this protein appear normal by electron microscopy examination (Botstein et al., 1973). P16 is essential when the particle infects a cell in the following cycle of infection (Botstein et al., 1973; King et al., 1973). We have characterized a mutant of P22 carrying a temperature-sensitive allele of gene 16. This mutant has previously been referred to as P22 25-ts (Levine et al., 1970, 1972) and P22 X-ts (Bezdek and Soska, 1970, 1973). P22 16-ts behaves as an early mutant at the nonpermissive temperature. Temperature shift experiments show that P16 of the infecting virion acts within the first 10 min at 25 C and that gene 16 product is required late in the latent period for incorporation into infectious phage. Induction does not require P16 for the production of particles. Particles produced either in a P22 16-ts thermal shift-up infection or after induction of 16-ts lysogens at 41 C are missing P16 and are, therefore, defective. P16 in P22 16-ts virions formed at the permissive temperature appears to be heat labile; it is inactivated after infection at 41 C. A simple assay for defective particles based on a complementation test is described.

“…This complex, intermediate I, is an association of parental phage DNA, newly synthesized phage DNA, and other cell constituents. In a previous paper we have shown that, upon superinfection of P22 lysogens with the homoimmune phage, the input phage DNA does not associate with intermediate I (9). That this inhibition is due to the action of repressor was shown by good association of the superinfecting DNA with the complex after induction with ultraviolet light.…”

mentioning

confidence: 94%

Virulent Mutants of Bacteriophage P22 I. Isolation and Genetic Analysis

Bronson

Levine

1971

Self Cite

Mutants of phage P22 which form plaques on a P22 lysogen have been isolated. These virulent mutants have been classified into three groups. (i) VirA mutants arise spontaneously in wild-type stocks and form very small turbid plaques on a P22 lysogen. The single mutation responsible for VirA virulence maps near the mnt locus, one of the immunity regions of phage P22. (ii) VirB mutants do not arise spontaneously and have been isolated only from mutagenized P22 stocks. VirB mutants form small, clear plaques on a P22 lysogen. One of the VirB mutants, virB-3, was analyzed in detail. The virB-3 mutant is comprised of two mutations: K5, which maps within the c2 gene, and Vx, which maps in the region between the c2 and c3 genes. Phages carrying either the K5 or Vx mutation are not virulent in themselves but mutate to VirB virulence at a frequency of 10-5 to 10-6. It is concluded that K5 and Vx are mutations at specific sites which together confer the ability to undergo phage development in the presence of repressor. (iii) VirC mutants are defined by a large clear plaque morphology when plated on a P22 lysogen. VirC mutants are comprised of the determinants of both VirA and VirB virulence.