Abstract

Growth experiments on the marine bacterium Vibrio angustum S14 were conducted under four light conditions using a solar simulator: visible light (V), V + ultraviolet A (UV-A), V + UV-A + UV-B radiation, and dark. Growth was inhibited mainly by UV-B and slightly by UV-A. UV-B radiation induced filaments containing multiple genome copies with low cyclobutane pyrimidine dimers. These cells did not show modifications in cellular fatty acid composition in comparison with dark control cultures and decreased in size by division after subsequent incubation in the dark. A large portion of the bacterial population grown under visible light showed an alteration in cellular DNA fluorescence as measured by flow cytometry after SYBR-Green I staining. This alteration was not aggravated by UV-A and was certainly due to a change in DNA topology rather than DNA deterioration because all the cells remained viable and their growth was not impaired. Ecological consequences of these observations are discussed.

Highlights

  • Marine bacteria are the main contributors in the transfer of carbon from the dissolved phase into the particulate phaseM

  • Bacterial Strain and Growth Experiments Under Simulated Solar Exposure V. angustum S14 (UNSW, Sydney, Australia) was grown in an artificial seawater medium supplemented with 3 mM D-glucose (ASW-G) [8] at 30°C with orbital shaking at 130 rpm

  • Four light treatments were studied simultaneously: (i) full radiation, (ii) visible light and ultraviolet A (UV-A), (iii) visible light, and (iv) dark

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Summary

Introduction

Marine bacteria are the main contributors in the transfer of carbon from the dissolved phase into the particulate phaseM. Solar radiation may have detrimental effects on bacteria by reducing DNA and protein synthesis, exoenzymatic activity and respiration Exposure to UV-B mainly has a direct effect on DNA by inducing dimerization of DNA bases and blocking DNA transcription and replication. The effects of exposure to UV-A, and to a lesser visible light (400–700 nm), are mainly indirect, by generation of reactive oxygen species (ROS) which interact with DNA, proteins, and lipids to induce damages that may be lethal or mutagenic [9]. Bacteria can efficiently repair UV-induced DNA damage by (i) photoreactivation after activation of the photolyase enzyme by light in the range of 380–430 nm and (ii) ‘‘dark’’ DNA repair mechanisms including nucleotideexcision repair, SOS-error-prone repair, and postreplication recombinational repair

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