Genetic evidence for a phosphorylation-independent signal transduction mechanism within the Bacillus subtilis stressosome.
Genetic evidence for a phosphorylation-independent signal transduction mechanism within the Bacillus subtilis stressosome.
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DOI：
10.1371/journal.pone.0090741
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Price CW
中科院分区：
文献类型：
--
作者：
Gaidenko TA;Price CW
应激体是一种 1.8 MDa 的细胞质复合物，控制多种细菌信号传导途径。它的作用在枯草芽孢杆菌中得到了最好的理解，它激活 σB 转录因子以应对各种严峻的环境挑战，包括酸、乙醇、热或盐胁迫。然而，应激体内信号传导机制的细节仍不确定。该复合物的核心包含 RsbR 共拮抗剂家族的一个或多个成员以及 RsbS 拮抗剂蛋白，该蛋白在没有应激的情况下结合 RsbT 激酶。作为响应的一部分，RsbT 首先磷酸化 T171 上的 RsbRA 共拮抗剂，然后磷酸化 S59 上的 RsbS；后一事件与应激诱导的 RsbT 释放相关，从而激活下游信号传导。在这里，我们检查了模型菌株中 S59 磷酸化的体内结果，该模型菌株的应激体核心仅由 RsbRA 共拮抗剂和 RsbS 形成。 RsbS 中磷酸化缺陷的 S59A 取代会阻碍对轻度应激的反应，但随着应激的增加，其影响逐渐减弱：S59A 的强乙醇攻击反应比野生型 RsbS 的反应强 60%。遗传分析将这种不依赖于 S59 的激活范围缩小到应激体，并确定在同时具有 T171A 和 S59A 取代的菌株中仍然存在显着的信号传导。我们推断 S59 磷酸化会提高信号效率，但不是必需的，并且在其不存在的情况下，第二种（或潜在的）信号转导机制占主导地位。这种解释使应激体信号传导仅通过控制 RsbT 激酶对 S59 的活性来介导的模型无效。
The stressosome is a 1.8 MDa cytoplasmic complex that controls diverse bacterial signaling pathways. Its role is best understood in Bacillus subtilis, where it activates the σB transcription factor in response to a variety of sharp environmental challenges, including acid, ethanol, heat or salt stress. However, details of the signaling mechanism within the stressosome remain uncertain. The core of the complex comprises one or more members of the RsbR co-antagonist family together with the RsbS antagonist protein, which binds the RsbT kinase in the absence of stress. As part of the response, RsbT first phosphorylates the RsbRA co-antagonist on T171 and then RsbS on S59; this latter event correlates with the stress-induced release of RsbT to activate downstream signaling. Here we examine the in vivo consequence of S59 phosphorylation in a model strain whose stressosome core is formed solely with the RsbRA co-antagonist and RsbS. A phosphorylation-deficient S59A substitution in RsbS blocked response to mild stress but had declining impact as stress increased: with strong ethanol challenge response with S59A was 60% as robust as with wild type RsbS. Genetic analysis narrowed this S59-independent activation to the stressosome and established that significant signaling still occurred in a strain bearing both the T171A and S59A substitutions. We infer that S59 phosphorylation increases signaling efficiency but is not essential, and that a second (or underlying) mechanism of signal transduction prevails in its absence. This interpretation nullifies models in which stressosome signaling is solely mediated by control of RsbT kinase activity toward S59.
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