Engelmann S, Hecker M
Institut für Mikrobiologie und Molekularbiologie, Greifswald, Germany.
FEMS Microbiol Lett. 1996 Nov 15;145(1):63-9. doi: 10.1111/j.1574-6968.1996.tb08557.x.
Two catalases of B. subtilis have been studied which are subject to two different regulatory mechanisms. Whereas KatA belongs to the group of proteins specifically induced by oxidative stress, KatE is a general delta B-dependent stress protein, not induced by oxidative stress. There are two mechanisms of oxidative stress resistance, the adaptive resistance induced by low H2O2 concentrations and an unspecific resistance acquired in glucose-starved cells. Mutants lacking KatA are defective in the adaptive resistance and both exponentially growing and glucose-starved cells are 100-fold more sensitive against lethal concentrations of H2O2. Under both conditions, however, a katE mutant was just as resistant as the wild type. Therefore, the role of KatE in oxidative stress tolerance remains obscure. sigB mutants which are no longer able to induce delta B-dependent general stress proteins in glucose-starved cells are characterized by a strong impairment in the unspecific oxidative stress resistance but not in the H2O2-induced oxidative stress resistance. This is the first evidence that sigB mutants have an obvious phenotype compared to the wild type and indicates that delta B-dependent general stress proteins may function in providing starving cells with resistance against oxidative stress.
已对枯草芽孢杆菌的两种过氧化氢酶进行了研究,它们受两种不同的调控机制支配。KatA属于由氧化应激特异性诱导的蛋白质组,而KatE是一种一般的依赖δB的应激蛋白,不受氧化应激诱导。存在两种抗氧化应激机制,即由低浓度过氧化氢诱导的适应性抗性和在葡萄糖饥饿细胞中获得的非特异性抗性。缺乏KatA的突变体在适应性抗性方面存在缺陷,指数生长期和葡萄糖饥饿的细胞对致死浓度的过氧化氢的敏感性要高100倍。然而,在这两种情况下,katE突变体的抗性与野生型一样。因此,KatE在氧化应激耐受性中的作用仍不清楚。sigB突变体在葡萄糖饥饿细胞中不再能够诱导依赖δB的一般应激蛋白,其特征是在非特异性氧化应激抗性方面有严重损伤,但在过氧化氢诱导的氧化应激抗性方面没有。这是第一个表明sigB突变体与野生型相比具有明显表型的证据,表明依赖δB的一般应激蛋白可能在为饥饿细胞提供抗氧化应激能力方面发挥作用。