I-017Recent 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.This work was part of the Virtual Institute for Microbial Stress and Survival supported by
the U. S. Department of Energy, Office of Science, Office of Biological and
Environmental Research, Genomics Program:GTL through contract DE-AC03-
76SF00099 between Lawrence Berkeley National Laboratory and the U. S. Department
of Energy
