Effects of Ultraviolet Radiation on Respiration and Growth in Radiation-resistant and Radiation-sensitive Strains of Escherichia coli B

Author:

Hamkalo Barbara A.1,Swenson P. A.2

Affiliation:

1. Department of Zoology, the University of Massachusetts, Amherst, Massachusetts

2. Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830

Abstract

Ultraviolet (UV) irradiation at 254 nm causes different respiration and growth responses in log-phase cultures of Escherichia coli B/r and B s−1 . These differences are correlated with the ability and inability, respectively, of these bacterial strains to repair UV-induced lesions in deoxyribonucleic acid (DNA). After irradiation, B s−1 cells (radiation-sensitive) exhibit uncoupling of growth and respiration; growth and synthesis cease, whereas respiration continues. B/r cells (radiation-resistant) grown on glycerol exhibit severe temporary inhibition of growth and respiration after UV, and the coupling of these two processes is maintained, except at a very high UV dose. Inhibition begins at about the time DNA synthesis resumes and continues for a period of time that is dependent upon dose. Glucose-grown cells do not exhibit severe respiratory, growth, and synthetic inhibitions; these processes remain coupled in the cells during the postirradiation period. Photoreactivation treatment delays uncoupling of growth and respiration in B s−1 and prevents inhibition of respiration and growth in B/r. These results indicate that the postirradiation responses result from the presence of pyrimidine dimers in DNA. Ultraviolet irradiation of B/r and B s−1 cells results in an accumulation of adenosine triphosphate by 30 min after UV. This accumulation decreases with time and does not appear to be related to the inhibition of respiration in glycerol-grown B/r cells. The results on B/r are interpreted in terms of a control mechanism for reestablishment of a balance among macromolecules in the irradiated cells so as to provide them with the potential to survive. The specific steps in such a reestablishment of balance appear to depend upon the substrate oxidized. In B s−1 cells, which cannot repair UV-induced damage in DNA, some control mechanism that coordinates cellular processes may be inactivated.

Publisher

American Society for Microbiology

Subject

Molecular Biology,Microbiology

Reference28 articles.

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4. Release of ultraviolet light-induced thymine dimers from DNA in E. coil K-12;Boyce R. P.;Proc. Nat. Acad. Sci. U.S.A.,1964

5. Dean A. C. R. and C. Hinshelwood. 1966. Growth function and regulation in bacterial cells. Clarendon Press Oxford.

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