Evidence for chloramphenicol-insensitive recA+-dependent single-stranded DNA repair
About: This article is published in Mutation Research.The article was published on 1980-08-01. It has received 1 citations till now. The article focuses on the topics: Nucleotide excision repair & Postreplication repair.
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TL;DR: Features of inactivation, repair and concomitant mutagenesis of hydroxylamine-treated phi X174 bacteriophages are reported here and possible mechanisms of these novel features are discussed.
Abstract: Features of inactivation, repair and concomitant mutagenesis of hydroxylamine- treated θX174 bacteriophages are reported here. (1) For reasons unknown, the nonsense phage mutants tested here were far more sensitive to hydroxylamine than the wild-type phage. In contrast, the sensitivities of these same θX174 mutants to UV-irradiation are indistinguishable. (2) Hydroxylamine-treated amber phages mutated to ochre but not to wild-type particles, i.e., G → A transition events were recovered. (3) The repair of θX174 phages from hydroxylamine-induced damage was error-prone, but unlike UV damage, did not require protein synthesis de novo. Possible mechanims of these novel features are discussed.
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TL;DR: The SOS repair hypothesis has already served as the working hypothesis for many experiments, and some speculations are presented to stimulate further discussions and experimental tests.
Abstract: A hypothesis was proposed several years ago that Escherichia coli possesses an inducible DNA repair system (“SOS repair”) which is also responsible for induced mutagenesis. Some characteristics of the SOS repair are (1) it is induced or activated following damage to DNA, (2) it requires de novo protein synthesis, (3) it requires several genetic functions of which the best-studied are recA + and lex + of E. coli, and (4) the physiological and genetic requirements for the expression of SOS repair are suspiciously similar to those necessary for the prophage induction. The SOS repair hypothesis has already served as the working hypothesis for many experiments, some of which are briefly reviewed. Also, some speculations are presented to stimulate further discussions and experimental tests.
656 citations
TL;DR: Induction kinetics and the half life of the inducible mutagenic DNA repair (SOS-repair) in E. coli have been determined using phage λ assays using ultraviolet induction patterns that very much resembles that of λ prophage in lysogenic induction.
Abstract: Ultraviolet mutagenesis of phage λ is produced by host functions which are inducible by ultraviolet irradiation of the host cell Induction kinetics and the half life of the inducible mutagenic DNA repair (SOS-repair) in E coli have been determined using phage λ assays At 37°C, both mutagenic and repair activities are maximal approximately 30 min following irradiation and decay with a half life of approximately 30 min The presence of 100 μg/ml chloramphenicol during the first 40 min after irradiation completely abolishes induction of repair and mutagenesis The ultraviolet induction pattern of SOS repair very much resembles that of λ prophage in lysogenic induction (Monk and Kinross, 1975)
108 citations
TL;DR: Evidence is provided showing that neither of these mechanisms accounts for UV reactivation of phage lambda, which differs from the other repair processes in that it is inducible and error-prone.
Abstract: Recovery of phage λ from ultraviolet damage can occur, in the dark, through three types of repair processes as defined by microbiological tests: (1) host-cell reactivation, (2) prophage reactivation, and (3) UV reactivation. This paper reviews the properties of the three repair processes, analyzes their dependence on the functioning of bacterial and phage genes, and discusses their relationship.
47 citations
TL;DR: Results indicate that the 4-semicarbazido-2-ketopyrimidine residue is also mutagenic but is less lethal than the corresponding 5,6-dihydro-6-sulfonate structure.
22 citations
TL;DR: Although nicking of the DS DNA molecule is an essential step even in the normal intracellular replication of ϕX DNA, the production and the sealing up of such nicks appear not to have any positive correlation with UVR of these phages.
Abstract: When UV-irradiated ϕX174 was grown in pre-irradiated host cells of various strains, “ultraviolet reactivation” (UVR) was observed only in recombination proficient strains such as E. coli C (uvrA+recA+) and HF4704 (uvrA-recA+), but not in the recombination deficient strain HF4712 (uvrA+recA-). By increasing the multiplicity of infection, no rise in the amount of such reactivation was observed. From the study of the neutral and alkaline sucrose gradient sedimentation patterns of DNA samples extracted from unirradiated cells infected with unirradiated phage, it appears that after the conversion of the viral single stranded (SS) DNA to the double stranded form (DS), “nicks” or scissions were produced on it within all three strains, which were ultimately sealed up in the recA+ but persisted within the recA- host cells. When UV-irradiated phage infected unirradiated host cells, such nicking of the DS DNA appeared to be much more extensive in uvrA+recA+, but slightly reduced in uvrA+recA- and severely suppressed in uvrA-recA+ strains. When the host cells were also UV-irradiated, the conversion of the infecting viral SS DNA to DS DNA as well as its subsequent nicking were reduced in all the three strains to a much greater extent. Although nicking of the DS DNA molecule is an essential step even in the normal intracellular replication of ϕX DNA, the production and the sealing up of such nicks appear not to have any positive correlation with UVR of these phages. A drastic reduction in nicking due te pre-irradiation of the host cells might, however, mean slowing down of the replication of the damaged parental RF molecules which would facilitate their repair perhaps through recombination with the homologous parts of the host genome.
21 citations