Relation Between Survival and Deoxyribonucleic Acid Replication in Ultraviolet-irradiated Resistant and Sensitive Strains of Escherichia Coli B-r

Overview

Journal J Bacteriol

Publisher American Society for Microbiology

Specialty Microbiology

Date 1973 Mar 1

PMID 4570772

Citations 6

Authors

J M Rude

C O DOUDNEY

Affiliations

Soon will be listed here.

Abstract

When arabinose-grown Escherichia coli B/r is ultraviolet (UV) irradiated in the logarithmic phase of growth, the dose inactivation curve for both colony formation and deoxyribonucleic acid (DNA) synthesis (based on the relative rates of synthesis) is exponential in nature. When protein synthesis is inhibited before UV-irradiation, both inactivation curves have a large shoulder. Pre-irradiation inhibition of protein synthesis increases considerably the colony-forming ability of a UV-irradiated Hcr(-) and Rec(-) strain of E. coli B/r. However, with the repair-deficient strains, both the shoulder and slope of the survival curve are affected. We investigated the effect of UV irradiation on DNA synthesis in Hcr(-) bacteria and found that pre-irradiation inhibition of protein synthesis increases UV resistance of DNA replication in this strain also. The results suggest that inhibition of protein synthesis before irradiation increases UV resistance in E. coli B/r by a mechanism which is independent of both the excision and recombination repair systems.

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DNA synthesis in pretreated and ultraviolet-irradiated cells of Escherichia coli B/r Her+ and Hcr-.

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Loss of photoreversibility of damage to deoxyribonucleic acid replication in ultraviolet-irradiated Escherichia coli B-r thy trp.

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PMID: 4607425 PMC: 245775. DOI: 10.1128/jb.120.1.394-398.1974.

Effect of preirradiation ribonucleic acid synthesis inhibition on resistance to ultraviolet light with resistant and sensitive strains of Escherichia coli B-r.

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PMID: 4600696 PMC: 245581. DOI: 10.1128/jb.119.1.123-128.1974.

Complexity of the ultraviolet mutation frequency response curve in Escherichia coli B/r: SOS induction, one-lesion and two-lesion mutagenesis.

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