Salt Stress in Desulfovibrio Vulgaris Hildenborough: An Integrated Genomics Approach
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Recent interest in the ability of Desulfovibrio vulgaris Hildenborough to reduce, and therefore contain, toxic and radioactive metal waste, has made all factors that affect its physiology of great interest. Increased salinity constitutes an important and frequent fluctuation faced by D. vulgaris in its natural habitat. In liquid culture, exposure to excess salt resulted in a striking cell elongation in D. vulgaris. Using data from transcriptomics, proteomics, metabolite assays, phospholipid fatty acid profiling, and electron microscopy, we undertook a systems approach to explore the effects of excess NaCl on D. vulgaris. This study demonstrates that import of osmoprotectants such as glycine betaine and ectoine constitute the primary mechanism used by D. vulgaris to counter hyper-ionic stress. Several efflux systems were also highly up-regulated, as was the ATP synthesis pathway. Increase in both RNA and DNA helicases suggested that salt stress had affected the stability of nucleic acid base pairing. An overall increase in branched fatty acids indicated changes in cell wall fluidity. An immediate response to salt stress included upregulation of chemotaxis genes though flagellar biosynthesis was down-regulated. Other down-regulated systems included lactate uptake permeases and ABC transport systems. The extensive NaCl stress analysis was compared with microarray data from KCl stress and unlike many other bacteria, D. vulgaris responded similarly to the two stresses. Integration of data from multiple methods has allowed us to present a conceptual model for salt stress response in D. vulgaris that can be compared to other microorganisms.