RpoS 介导的大肠杆菌一般性应激反应。
The RpoS-mediated general stress response in Escherichia coli.
机构信息
Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892, USA.
出版信息
Annu Rev Microbiol. 2011;65:189-213. doi: 10.1146/annurev-micro-090110-102946.
Under conditions of nutrient deprivation or stress, or as cells enter stationary phase, Escherichia coli and related bacteria increase the accumulation of RpoS, a specialized sigma factor. RpoS-dependent gene expression leads to general stress resistance of cells. During rapid growth, RpoS translation is inhibited and any RpoS protein that is synthesized is rapidly degraded. The complex transition from exponential growth to stationary phase has been partially dissected by analyzing the induction of RpoS after specific stress treatments. Different stress conditions lead to induction of specific sRNAs that stimulate RpoS translation or to induction of small-protein antiadaptors that stabilize the protein. Recent progress has led to a better, but still far from complete, understanding of how stresses lead to RpoS induction and what RpoS-dependent genes help the cell deal with the stress.
在营养缺乏或应激条件下，或者当细胞进入静止期时，大肠杆菌和相关细菌会增加特殊 sigma 因子 RpoS 的积累。RpoS 依赖性基因表达导致细胞的普遍应激抗性。在快速生长期间，RpoS 翻译受到抑制，并且合成的任何 RpoS 蛋白都会迅速降解。通过分析特定应激处理后 RpoS 的诱导，已经部分解析了从指数生长到静止期的复杂转变。不同的应激条件导致特定的 sRNA 的诱导，这些 sRNA 刺激 RpoS 翻译，或者导致小蛋白反适应子的诱导，从而稳定蛋白质。最近的进展使人们对应激如何导致 RpoS 的诱导以及 RpoS 依赖性基因如何帮助细胞应对应激有了更好的理解，但仍远未完全理解。
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