Inhibitory Effect of Bacteriophage P22 Infection on Host Cell Deoxyribonuclease Activity

Israel, Vance; Woodworth-Gutai, M; Levine, Fred

doi:10.1128/jvi.9.5.752-757.1972

Cited by 11 publications

(3 citation statements)

References 16 publications

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“…Specifically, bacteriophages lambda and T4 inactivate this enzyme in E. coli (38,40). Similarly, nuclease inactivation has also been demonstrated in Salmonella after infection with bacteriophage P22 (26). In Staphylococcus aureus (37), transformation requires lysogeny.…”

Section: Discussionmentioning

confidence: 93%

Effect of lysogeny on transfection and transfection enhancement in Bacillus subtilis

Yasbin¹,

Wilson²,

Young³

1975

J Bacteriol

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Strains of Bacillus subtilis 168 lysogenic for bacteriophage 0105 transfect with deoxyribonucleic acid (DNA) isolated from bacteriophage SP02 at a higher efficiency than non-lysogenic strains. This enhancement of transfection was not the result of recombination between bacteriophages SP02 and 0105. Superinfection marker rescue increased transfection with DNA from bacteriophage SP02 when infection with either bacteriophage SPO2sus6 or bacteriophage 0105 occurred simultaneously with the addition of the transfecting DNA. Again, this enhancement of transfection was not the result of recombination but rather a protection of the transfecting DNA by the superinfecting bacteriophage. The ability of the superinfecting bacteriophage to protect the transfecting DNA from inactivation was maximal when the bacteria were just becoming competent. Bacteriophage cannot replicate after the transfection of competent bacteria lacking a functional DNA replication system, whereas bacteriophage 41 was able to replicate after infection of competent bacteria grown under comparable conditions. These observations support the hypothesis that GAPase and an inducible repair system play an important role in the development of competence.

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Section: Discussionmentioning

confidence: 93%

Effect of lysogeny on transfection and transfection enhancement in Bacillus subtilis

Yasbin¹,

Wilson²,

Young³

1975

J Bacteriol

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“…Co-infections showed that gp16 can work in trans, complementing a gp16-deficient particle, indicating that its essential early function occurs once DNA is ejected inside the host. Furthermore, gp16 deficient phage do not induce the superinfection exclusion response and gp16 is not part of the replication machinery [ 162 ]. Indirect evidence supports a membrane-breaching role, as purified gp16 disrupts dye-loaded, lipid vesicles [ 163 ].…”

Section: Bubblegrams and Cryo-et Reveal Asymmetrically Organized Pmentioning

confidence: 99%

Breaking Symmetry in Viral Icosahedral Capsids as Seen through the Lenses of X-ray Crystallography and Cryo-Electron Microscopy

Parent

Schrad

Cingolani

2018

Viruses

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The majority of viruses on Earth form capsids built by multiple copies of one or more types of a coat protein arranged with 532 symmetry, generating an icosahedral shell. This highly repetitive structure is ideal to closely pack identical protein subunits and to enclose the nucleic acid genomes. However, the icosahedral capsid is not merely a passive cage but undergoes dynamic events to promote packaging, maturation and the transfer of the viral genome into the host. These essential processes are often mediated by proteinaceous complexes that interrupt the shell’s icosahedral symmetry, providing a gateway through the capsid. In this review, we take an inventory of molecular structures observed either internally, or at the 5-fold vertices of icosahedral DNA viruses that infect bacteria, archea and eukaryotes. Taking advantage of the recent revolution in cryo-electron microscopy (cryo-EM) and building upon a wealth of crystallographic structures of individual components, we review the design principles of non-icosahedral structural components that interrupt icosahedral symmetry and discuss how these macromolecules play vital roles in genome packaging, ejection and host receptor-binding.

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“…Infections in the absence of functional P16. The following features of infection in the absence of functional P16 are well established: (i) adsorption proceeds with normal kinetics and (ii) phage DNA is at least partially released from the capsid; (iii) the host cells are not detectably affected; they continue to grow and divide with the same kinetics as uninfected cells (6; Hoffman, Ph.D. thesis); (iv) no change in the rate of DNA synthesis in the infected culture is observed, suggesting that no phage DNA is synthesized (6; Hoffman, Ph.D. thesis); (v) the parental phage DNA does not associate with the replication complex (23); (vi) these infections do not result in the transcription of any phage-specific RNA, as determined by RNA-DNA hybridization (E. N. Jackson, personal communication); (vii) superinfection exclusion is not induced; (viii) no phage protein synthesis is detected (15); (ix) two alterations in enzymatic activity are detected early in P22 infections-a loss of host DNase activity specific for denatured DNA (15) and an increase in phage-specified DNase activity specific for native DNA (36); infections in the absence of P16 activity fail to show either of these effects; and (x) the host cannot be lysogenized. Thus, in the absence of functional P16, there is a block at an early step in the infective process which prevents the expression of any phage functions following at least partial release of phage DNA from the capsid.…”

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confidence: 99%

Bacteriophage P22 virion protein which performs an essential early function. II. Characterization of the gene 16 function

Hoffman¹,

Levine²

1975

J Virol

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P16 is a virion protein and, as such, is incorporated into the phage head as a step in morphogenesis. The role of P16 in assembly is not essential since particles are formed without this protein which appear normal by electron microscopy. P16 is essential when the particle infects a cell in the following cycle of infection. In the absence of functional P16, the infection does not appear to proceed beyond release of phage DNA from the capsid. No known genes are expressed, no DNA is transcribed, and the host cell survives the infection, continuing to grow and divide normally. The P16 function is required only during infection for the expression of phage functions. Induction in the absence of P16 proceeds with the expression ofearly and late genes and results in particle formation. P16 must be incorporated during morphogenesis into progeny particles after both infection and induction for the progeny to be infectious. The P16 function is necessary for transduction as well as for infection. Its activity is independent of new protein synthesis and it is not under immunity control. P16 can act in trans, but appears to act preferentially on the phage or phage DNA with which it is packaged. The data from complementation studies are compatible with P16 release from the capsid with the phage DNA. In the absence of P16 the infection is blocked, but the phage genome is not degraded. The various roles which have been ruled out for P16 are: (i) an early regulatory function, (ii) an enzymatic activity necessary for phage production, (iii) protection of phage DNA from host degradation enzymes, (iv) any generalized alteration of the host cell, (v) binding parental DNA to the replication complex, and (vi) any direct involvement in the replication of P22 DNA. P16 can be responsible for: (i) complete release of the DNA and disengagement from the capsid, (ii) bringing the released DNA to some necessary cell site or compartment such as the cytoplasm, (iii) removal of other virion proteins from the injected DNA, and (iv) alterations of the structure of the injected DNA.

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Inhibitory Effect of Bacteriophage P22 Infection on Host Cell Deoxyribonuclease Activity

Cited by 11 publications

References 16 publications

Effect of lysogeny on transfection and transfection enhancement in Bacillus subtilis

Effect of lysogeny on transfection and transfection enhancement in Bacillus subtilis

Breaking Symmetry in Viral Icosahedral Capsids as Seen through the Lenses of X-ray Crystallography and Cryo-Electron Microscopy

Bacteriophage P22 virion protein which performs an essential early function. II. Characterization of the gene 16 function

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