Deoxyribonucleic acid repair in bacteriophage.

Bernstein, Carol

doi:10.1128/mmbr.45.1.72-98.1981

Cited by 41 publications

(14 citation statements)

References 117 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Over the past two decades it has been established that many mutagens are capable of producing directly, or after metabolic activation, a variety of DNA structural lesions that are subject to various modes of DNA repair [Hanawalt et al, 1979;Wright, 1980;Bernstein, 1981;Haynes and Kunz, 19811. These repair processes can be divided operationally into two categories-error-free repair (EFR) and error-prone repair (EPR).…”

Section: Introductionmentioning

confidence: 99%

Genetic effects of deoxyribonucleotide pool imbalances

Kunz

1982

Environ. mutagen

124

View full text Add to dashboard Cite

In vivo DNA precursor imbalances can have profound genetic consequences in prokaryotes and eukaryotes. In vitro studies have demonstrated that DNA replication fidelity is dependent on correct balances of deoxyribonucleoside triphosphates during DNA synthesis. These findings suggest that intracellular concentrations of DNA precursors may be regulated in order to minimize the frequency of genetic change. In addition, they indicate the existence of important nonDNA targets for the induction of mutation, recombination, chromosome aberrations, etc. In this article, the genetic effects of deoxyribonucleotide pool imbalances are reviewed.

show abstract

Section: Introductionmentioning

confidence: 99%

Genetic effects of deoxyribonucleotide pool imbalances

Kunz

1982

Environ. mutagen

124

View full text Add to dashboard Cite

show abstract

“…DNA damage in bacterial and algal cells can be repaired by light-dependent (photoreactivation) as well as light-independent (dark repair) mechanisms. While some viruses encode for their own DNA repair enzymes (17,18), most viruses rely on the DNA repair mechanisms of host cells (2). While the loss of infectivity associated with exposure to UV radiation is typically caused by damage to the viral DNA, repair is possible only after the DNA has been injected into the host cell.…”

mentioning

confidence: 99%

Photoreactivation compensates for UV damage and restores infectivity to natural marine virus communities

Weinbauer

Wilhelm

Suttle

et al. 1997

Appl Environ Microbiol

View full text Add to dashboard Cite

We investigated the potential for photoreactivation to restore infectivity to sunlight-damaged natural viral communities in offshore (chlorophyll a, <0.1 g liter ؊1), coastal (chlorophyll a, ca. 0.2 g liter ؊1), and estuarine (chlorophyll a, ca. 1 to 5 g liter ؊1) waters of the Gulf of Mexico. In 67% of samples, the lightdependent repair mechanisms of the bacterium Vibrio natriegens restored infectivity to natural viral communities which could not be repaired by light-independent mechanisms. Similarly, exposure of sunlight-damaged natural viral communities to >312-nm-wavelength sunlight in the presence of the natural bacterial communities restored infectivity to 21 to 26% of sunlight-damaged viruses in oceanic waters and 41 to 52% of the damaged viruses in coastal and estuarine waters. Wavelengths between 370 and 550 nm were responsible for restoring infectivity to the damaged viruses. These results indicate that light-dependent repair, probably photoreactivation, compensated for a large fraction of sunlight-induced DNA damage in natural viral communities and is potentially essential for the maintenance of high concentrations of viruses in surface waters.

show abstract

“…It probably also acts on hmC-containing DNA, since general phage recombination is dependent upon gene 46 infection (4,7). Other processes, such as certain DNA repair pathways and the second stage of phage DNA replication, are thought to involve recombination because of their dependence on gene 46 function (3,8,36). It seems natural to associate the cleavage at M with one or more of these gp 46-associated pathways or with the consequence of the failure of gp 46 to function in one of these pathways.…”

Section: Discussionmentioning

confidence: 99%

Site-specific cleavage of bacteriophage T4 DNA associated with the absence of gene 46 product function

Albright¹,

Geiduschek²

1983

J Virol

View full text Add to dashboard Cite

A plasmid containing a copy of the late gene 23 was cleaved at two specific locations after bacteriophage T4 infection. Cleavage at the major site, which is at the 3' end of gene 23, was detected only in the absence of gene 46 product function and was independent of the state of modification of cytosine residues. Cutting of plasmid (cytosine-containing) DNA at this site was independent of phage DNA replication and late transcription functions. A second cleavage site, in vector DNA, was also mapped. The minor extent of cutting at this site was independent of gene 46 function. Gene 46 codes for, or controls, an exonuclease involved in T4 DNA recombination and in degradation of cytosine-containing DNA. The coupling of transcription of bacteriophage T4 late genes to replication of the viral DNA remains poorly understood, but some "activation" of the DNA template is thought to be provided by replication (37, 50). We have thought that some progress in defining the nature of DNA competence for late transcription could be made if one examined the effect of T4 infection on the structure of a plasmid containing a T4 late gene. We chose gene 23, which codes for the major capsid protein, for this purpose. Previous experiments have established that the plasmid-borne gene 23 is expressed late in infection and have defined some of the relevant parameters (16, 17). Analysis of deproteinized plasmid DNA uncovered an unexpected effect: a site-specific cleavage of T4 DNA occurred in the absence of gene 46 function. The gene 46 product is involved both in T4 recombination and in degradation of DNA. This report is concerned primarily with the site-specific cleavage. MATERIALS AND METHODS Media. M9S and tryptone broth have been described previously (6). H-2 (low phosphate) medium is medium B-2 of Studier (44), without phosphate, and with 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-NaOH (pH 7.5) in place of bis-Tris (G. Kassavetis, personal communicaion.). Bacteria. Escherichia coli CR63 and B40suI were

show abstract

Deoxyribonucleic acid repair in bacteriophage.

Cited by 41 publications

References 117 publications

Genetic effects of deoxyribonucleotide pool imbalances

Genetic effects of deoxyribonucleotide pool imbalances

Photoreactivation compensates for UV damage and restores infectivity to natural marine virus communities

Site-specific cleavage of bacteriophage T4 DNA associated with the absence of gene 46 product function

Contact Info

Product

Resources

About