Hecker M, Völker U
Ernst-Moritz-Arndt-Universität Greifwald, Institut für Mikrobiologie und Molekularbiologie, Greifswald, Germany.
Mol Microbiol. 1998 Sep;29(5):1129-36. doi: 10.1046/j.1365-2958.1998.00977.x.
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 sigmaB-dependent general stress regulon. Despite a good understanding of the complex regulation of the activity of sigmaB and knowledge of a very large number of general stress genes controlled by sigmaB, first insights into the physiological role of this nonspecific stress response have been obtained only very recently. To explore the physiological role of this reguIon, we and others identified sigmaB-dependent general stress genes and compared the stress tolerance of wild-type cells with mutants lacking sigmaB or general stress proteins. The proteins encoded by sigmaB-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 sigmaB-dependent dps gene encoding a DNA-protecting protein. Protection against oxidative damage of membranes, proteins or DNA could be the most essential component of sigmaB mediated general stress resistance in growth-arrested aerobic gram-positive bacteria. Other general stress genes have both a sigmaB-dependent induction pathway and a second sigmaB-independent mechanism of stress induction, thereby partially compensating for a sigmaB deficiency in a sigB mutant. In contrast to sigB mutants, null mutations in genes encoding those proteins, such as cIpP or cIpC, cause extreme sensitivity to salt or heat.
枯草芽孢杆菌细胞通过增加一般应激蛋白（GSPs）的产生，几乎能立即对不同的应激条件做出反应。编码大多数受热、乙醇、盐胁迫或葡萄糖、氧气或磷酸盐饥饿诱导的GSPs的基因，属于依赖σB的一般应激调节子。尽管对σB活性的复杂调节有了很好的理解，并且知道大量受σB控制的一般应激基因，但直到最近才首次深入了解这种非特异性应激反应的生理作用。为了探索这个调节子的生理作用，我们和其他人鉴定了依赖σB的一般应激基因，并比较了野生型细胞与缺乏σB或一般应激蛋白的突变体的应激耐受性。依赖σB的一般应激基因编码的蛋白质可分为至少五个功能组，它们很可能为生长受限的枯草芽孢杆菌细胞提供多重应激抗性，以应对未来的应激。特别是，σB突变体在对氧化应激的非特异性抗性方面受损，这需要依赖σB的dps基因，该基因编码一种DNA保护蛋白。对膜、蛋白质或DNA的氧化损伤的保护可能是生长停滞的需氧革兰氏阳性细菌中σB介导的一般应激抗性的最基本组成部分。其他一般应激基因既有依赖σB的诱导途径，也有第二种不依赖σB的应激诱导机制，从而部分补偿σB突变体中σB的缺陷。与σB突变体相反，编码这些蛋白质（如ClpP或ClpC）的基因中的无效突变会导致对盐或热极度敏感。
