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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Abstract— For E. coli B/r u.v.‐irradiated while in logarithmic growth, the nature of the dose‐response curve was strongly dependent on both pre‐ and post‐irradiation conditions of growth. Survival curves for cells grown in nutrient medium, or minimal medium with glucose, and plated immediately after irradiation, demonstrated an initial insensitive or ‘shoulder’ region provided the plating medium was such that no derepression was required of operons controlling inducible enzyme systems. If, however, such derepression was called for, survival curves were of exponential form. Delay in plating resulted in the return of the survival curve to the shouldered form even when ‘shift‐down’ media were used. Of those cells grown before u.v.‐irradiation in minimal media and plated thereafter with the same sugar as carbon source, only those grown with glucose (or lactose) demonstrated the shouldered survival curve.

The ultraviolet resistance of a streptolydigin-susceptible strain of Escherichia coli B/r hcr-increased during preirradiation treatment with streptolydigin (an inhibitor of deoxyribonucleic acid-dependent ribonucleic acid polymerase) for 20 min and then remained constant. During preirradiation treatment with chloramphenicol (an inhibitor of protein synthesis), resistance to ultraviolet light increased for 1 to 2 h, and reached a maximal level significantly above that attained in streptolydigin-containing medium. These results suggest that there are two mechanisms that function in Hcr-cells during chloramphenicol treatment which contribute to the concomitant ultraviolet resistance enhancement. One is ribonucleic acid dependent and is inhibited by streptolydigin. This ribonucleic acid-dependent mechanism appears to be absent in wild-type and RecA E. coli B/r strains.Experimental design and UV irradiation procedure. The logarithmic phase culture was either prepared immediately for UV irradiation or was subjected to onq of the following preirradiation treat-123 on August 1, 2020 by guest