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Non-specific, general and multiple stress resistance of growth-restricted Bacillus subtilis cells by the expression of the σB regulon
Authors:Michael Hecker  & Uwe Völker
Institution:Ernst-Moritz-Arndt-Universität Greifswald, Institut für Mikrobiologie und Molekularbiologie, F.-L.-Jahn-Straße 15, D-17487 Greifswald, Germany.,;Philipps-Universität Marburg, Laboratorium für Mikrobiologie und Max-Planck-Institut für terrestrische Mikrobiologie, Karl-von-Frisch-Straße, D-35043 Marburg, Germany.
Abstract:Bacillus subtilis cells respond almost immediately to different stress conditions by increasing the production of general stress proteins (GSPs). The genes encoding the majority of the GSPs that are induced by heat, ethanol, salt stress or by starvation for glucose, oxygen or phosphate belong to the σB-dependent general stress regulon. Despite a good understanding of the complex regulation of the activity of σB and knowledge of a very large number of general stress genes controlled by σB, first insights into the physiological role of this non-specific stress response have been obtained only very recently. To explore the physiological role of this regulon, we and others identified σB-dependent general stress genes and compared the stress tolerance of wild-type cells with mutants lacking σB or general stress proteins. The proteins encoded by σB-dependent general stress genes can be divided into at least five functional groups that most probably provide growth-restricted B. subtilis cells with a multiple stress resistance in anticipation of future stress. In particular, sigB mutants are impaired in non-specific resistance to oxidative stress, which requires the σB-dependent dps gene encoding a DNA-protecting protein. Protection against oxidative damage of membranes, proteins or DNA could be the most essential component of σB-mediated general stress resistance in growth-arrested aerobic Gram-positive bacteria. Other general stress genes have both a σB-dependent induction pathway and a second σB-independent mechanism of stress induction, thereby partially compensating for a σB deficiency in a sigB mutant. In contrast to sigB mutants, null mutations in genes encoding those proteins, such as clpP or clpC, cause extreme sensitivity to salt or heat.
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