Hengge-Aronis R
Department of Biology, University of Konstanz, Germany.
Mol Microbiol. 1996 Sep;21(5):887-93. doi: 10.1046/j.1365-2958.1996.511405.x.
It is now well established that the sigma S subunit of RNA polymerase is a master regulator in a complex regulatory network that governs the expression of many stationary-phase-inducible genes in Escherichia coli. In this review, more recent findings will be summarized that demonstrate that sigma S also acts as a global regulator for the osmotic control of gene expression, and actually does so in exponentially growing cells. Thus, many sigma S-dependent genes are induced during entry into stationary phase as well as in response to osmotic upshift. K+ glutamate, which accumulates in hyperosmotically stressed cells, seems to specifically stimulate the activity of sigma S-containing RNA polymerase at sigma S-dependent promoters. Moreover, osmotic upshift results in an elevated cellular sigma S level similar to that observed in stationary-phase cells. This increase is the result of a stimulation of rpoS translation as well as an inhibition of the turnover of sigma S, which in exponentially growing non-stressed cells is a highly unstable protein. Whereas the RNA-binding protein HF-I, previously known as a host factor for the replication of phage Q beta RNA, is essential for rpoS translation, the recently discovered response regulator RssB, and ClpXP protease, have been shown to be required for sigma S degradation. The finding that the histone-like protein H-NS is also involved in the control of rpoS translation and sigma S turnover, sheds new light on the function of this protein in osmoregulation. Finally, preliminary evidence suggests that additional stresses, such as heat shock and acid shock, also result in increased cellular sigma S levels in exponentially growing cells. Taken together, sigma S function is clearly not confined to stationary phase. Rather, sigma S may be regarded as a sigma factor associated with general stress conditions.
现已充分证实，RNA聚合酶的σS亚基是一个复杂调控网络中的主要调节因子，该网络控制着大肠杆菌中许多稳定期诱导基因的表达。在这篇综述中，将总结一些最新发现，这些发现表明σS也是基因表达渗透控制的全局调节因子，并且实际上在指数生长的细胞中也发挥着这种作用。因此，许多依赖σS的基因在进入稳定期以及应对渗透压升高时都会被诱导表达。在高渗应激细胞中积累的K⁺谷氨酸似乎能特异性地刺激依赖σS的启动子处含σS的RNA聚合酶的活性。此外，渗透压升高会导致细胞内σS水平升高，类似于在稳定期细胞中观察到的情况。这种增加是rpoS翻译受到刺激以及σS周转受到抑制的结果，在指数生长的非应激细胞中，σS是一种高度不稳定的蛋白质。虽然以前被称为噬菌体QβRNA复制宿主因子的RNA结合蛋白HF-I对rpoS翻译至关重要，但最近发现的应答调节因子RssB和ClpXP蛋白酶已被证明是σS降解所必需的。组蛋白样蛋白H-NS也参与rpoS翻译和σS周转的控制这一发现，为该蛋白在渗透调节中的功能提供了新的线索。最后，初步证据表明，其他应激，如热休克和酸休克，也会导致指数生长细胞中细胞内σS水平升高。综上所述，σS的功能显然不限于稳定期。相反，σS可被视为与一般应激条件相关的σ因子。
