Enhancement of Damage to Escherichia coli Strain B/R after Ultraviolet and   Irradiation

Forage, A. J.; Gillies, N. E.

doi:10.1099/00221287-59-3-329

Cited by 7 publications

(2 citation statements)

References 3 publications

(2 reference statements)

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“…Each of the three inhibitors of protein synthesis that we tested, chloramphenicol, puromycin, and deprivation of required amino acids, reduced the survival of "wild-type" E. coli K-12 after UV and X irradiation. These results are consistent with those reported by other investigators using other E. coli strains (1,2,8,14,24). Although Marshall and Gillies (22) reported that chloramphenicol caused no reduction in the survival of gamma-irradiated cells of K-12, we feel that differences between their experimental conditions and ours may account for the discrepancy.…”

Section: Discussionsupporting

confidence: 93%

“…Inhibitors of protein synthesis can reduce the survival of some strains of Escherichia coli following ultraviolet (UV) or ionizing radiation (1,2,8,14,22,24). We wished to determine whether strain K-12 was similarly affected, and, if so, whether the decrease in survival could be attributed to the inhibition of any of the systems responsible for repairing damage caused by UV or X radiation.…”

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Requirement for Protein Synthesis inrec-Dependent Repair of Deoxyribonucleic Acid inEscherichia coliafter Ultraviolet or X Irradiation

Ganesan

Smith

1972

J Bacteriol

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Deprivation of amino acids required for growth or treatment with chloramphenicol or puromycin after irradiation reduced the survival of Rec+ cells of Escherichia coli K-12 which had been exposed to either ultraviolet (UV) or X radiation. In contrast, these treatments caused little or no reduction in the survival of irradiated recA or recB mutants. The effect of chloramphenicol on the survival of X-irradiated cells was correlated with an inhibition of repair of single-strand breaks in irradiated deoxyribonucleic acid (DNA), previously shown to be controlled by recA and recB. In UV-irradiated cells no effect of chloramphenicol was detected on the repair of single-strand discontinuities in DNA replicated from UV-damaged templates, a process controlled by recA but not by recB. From this we concluded that inhibiting protein synthesis in UV or X-irradiated cells may interfere with some biochemical step in repair dependent upon the recB gene. When irradiated Rec+ cells were cultured for a sufficient period of time in minimal growth medium before chloramphenicol treatment their survival was no longer decreased by the drug. After X irradiation this occurred in less than one generation time of the unirradiated control cells. After UV irradiation it occurred more slowly and was only complete after several generation times of the unirradiated controls. These observations indicated that replication of the entire irradiated genome was probably not required for rec-dependent repair of X-irradiated cells, although it might be required for rec-dependent repair of UV-irradiated cells.

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Section: Discussionsupporting

confidence: 93%

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confidence: 99%

Requirement for Protein Synthesis inrec-Dependent Repair of Deoxyribonucleic Acid inEscherichia coliafter Ultraviolet or X Irradiation

Ganesan

Smith

1972

J Bacteriol

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Physiological Responses of Escherichia coli to Far-Ultraviolet Radiation

Swenson

1976

Photochemical and Photobiological Reviews

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Dependence of DNA dark repair on protein synthesis inEscherichia coli

1977

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We investigated the influence of amino-acidless treatments applied prior and after UV irradiation (AA-irradiated AA+; AA-irradiated A-; AA+ irradiated AA-) on survival, dimer excision, postirradiation DNA degradation, DNA synthesis and sedimentation profiles of parental DNA of E. coli B/r Hcr+ cells. In dependence on the treatment applied, the fluence 50 J/m2 yielded distinctly different fractions of survivors within 0,03-85%. In all cases dimers were completely excised. The rate of DNA degradation was similar during a 30-40 min period after UV during which the bulk of dimers was excised. Degradation ceased, however, earlier in the prestarved cells than in exponentially growing ones; it was prolonged by aminoacidless postincubation. Sedimentation profiles of parental DNA did not differ during the whole period of dimer excision. In AA+ AA- cells DNA synthesis was not restored for several hours after addition of amino acids. In AA- AA- cells addition of amino acids resulted in a fast resumption of DNA synthesis. We conclude that removal of dimers and repair of gaps were similar in all cases. We believe that aminoacidless treatments influence production and repair of damage to the sites of DNA replication. The treatment appears to prevent this damage when applied before UV irradiation, but interferes with its restoration when applied after UV irradiation. Consequently, the former treatment increases survival of cells while the latter produces an opposite effect.

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Enhancement of Damage to Escherichia coli Strain B/R after Ultraviolet and Irradiation

Cited by 7 publications

References 3 publications

Requirement for Protein Synthesis inrec-Dependent Repair of Deoxyribonucleic Acid inEscherichia coliafter Ultraviolet or X Irradiation

Requirement for Protein Synthesis inrec-Dependent Repair of Deoxyribonucleic Acid inEscherichia coliafter Ultraviolet or X Irradiation

Physiological Responses of Escherichia coli to Far-Ultraviolet Radiation

Dependence of DNA dark repair on protein synthesis inEscherichia coli

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