Spo0A∼P is the master regulator of sporulation in Bacillus subtilis. Activity of Spo0A is regulated by a phosphorelay integrating multiple positive and negative signals by the action of kinases and phosphatases. The phosphatase Spo0E specifically inactivates the response regulator Spo0A∼P by dephosphorylation. We identified a σB-type promoter adjacent to spo0E that is activated by the general stress response sigma factor σB and is responsible for spo0E induction in vivo. Ectopic expression of σB and subsequent induction of spo0E cause a σB-dependent block of sporulation-specific transcription of the spo0A and spoIIE genes and produces a sporulation-deficient phenotype. This effect could be erased by a deletion of the σB promoter of spo0E and thus solely addresses σB activity. Here, a molecular mechanism is shown that integrates σB activity into the decision-making process of sporulation and provides a link to interconnect these two dominant and probably mutually exclusive adaptive responses in the regulatory network of B. subtilis.
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机译：Spo0A〜P是枯草芽孢杆菌孢子形成的主要调节因子。 Spo0A的活性受激酶和磷酸酶作用下整合多个正信号和负信号的磷光体的调节。磷酸酶Spo0E通过去磷酸化使反应调节因子Spo0A〜P失活。我们确定了一个与spo0E相邻的σ B 型启动子，该启动子被一般应激反应sigma因子σ B 激活，并负责体内的spo0E诱导。 σ B 的异位表达和随后的spo0E的诱导导致spo0A和spoIIE基因的σ B 依赖的孢子特异性转录的阻滞，并产生了孢子形成缺陷的表型。可以通过删除spo0E的σ B 启动子来消除这种效应，从而仅解决σ B 活性。在这里，显示了一种分子机制，该机制将σ B 活性整合到孢子形成的决策过程中，并提供了一个链接，以将枯草芽孢杆菌的调控网络中的这两个主要且可能互斥的适应性反应相互连接。 。
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