Prágai Zoltán, Allenby Nicholas E E, O'Connor Nicola, Dubrac Sarah, Rapoport Georges, Msadek Tarek, Harwood Colin R
School of Cell and Molecular Biosciences, The Medical School, University of Newcastle upon Tyne, Framlington Place, Newcastle upon Tyne, NE2 4HH, United Kingdom.
J Bacteriol. 2004 Feb;186(4):1182-90. doi: 10.1128/JB.186.4.1182-1190.2004.
When Bacillus subtilis is subjected to phosphate starvation, the Pho regulon is activated by the PhoP-PhoR two-component signal transduction system to elicit specific responses to this nutrient limitation. The response regulator, PhoP, and its cognate histidine sensor kinase, PhoR, are encoded by the phoPR operon that is transcribed as a 2.7-kb bicistronic mRNA. The phoPR operon is transcribed from two sigma(A)-dependent promoters, P(1) and P(2). Under conditions where the Pho regulon was not induced (i.e., phosphate-replete conditions or phoR-null mutant), a low level of phoPR transcription was detected only from promoter P(1). During phosphate starvation-induced transition from exponential to stationary phase, the expression of the phoPR operon was up-regulated in a phosphorylated PhoP (PhoP approximately P)-dependent manner; in addition to P(1), the P(2) promoter becomes active. In vitro gel shift assays and DNase I footprinting experiments showed that both PhoP and PhoP approximately P could bind to the control region of the phoPR operon. The data indicate that while low-level constitutive expression of phoPR is required under phosphate-replete conditions for signal perception and transduction, autoinduction is required to provide sufficient PhoP approximately P to induce other members of the Pho regulon. The extent to which promoters P(1) and P(2) are activated appears to be influenced by the presence of other sigma factors, possibly the result of sigma factor competition. For example, phoPR is hyperinduced in a sigB mutant and, later in stationary phase, in sigH, sigF, and sigE mutants. The data point to a complex regulatory network in which other stress responses and post-exponential-phase processes influence the expression of phoPR and, thereby, the magnitude of the Pho regulon response.
当枯草芽孢杆菌遭遇磷酸盐饥饿时，Pho调控子会被PhoP - PhoR双组分信号转导系统激活，以引发对这种营养限制的特定反应。反应调节因子PhoP及其同源组氨酸传感器激酶PhoR由phoPR操纵子编码，该操纵子转录为2.7 kb的双顺反子mRNA。phoPR操纵子从两个依赖于σ(A)的启动子P(1)和P(2)转录。在Pho调控子未被诱导的条件下（即磷酸盐充足的条件或phoR基因缺失突变体），仅从启动子P(1)检测到低水平的phoPR转录。在磷酸盐饥饿诱导的从指数生长期到稳定期的转变过程中，phoPR操纵子的表达以磷酸化的PhoP（PhoPP）依赖的方式上调；除了P(1)，P(2)启动子也变得活跃。体外凝胶迁移试验和DNase I足迹实验表明，PhoP和PhoPP都能结合到phoPR操纵子的控制区域。数据表明，虽然在磷酸盐充足的条件下phoPR的低水平组成型表达对于信号感知和转导是必需的，但自诱导是提供足够的PhoP~P以诱导Pho调控子其他成员所必需的。启动子P(1)和P(2)被激活的程度似乎受其他σ因子的存在影响，这可能是σ因子竞争的结果。例如，phoPR在sigB突变体中过度诱导，在稳定期后期，在sigH、sigF和sigE突变体中也过度诱导。数据指向一个复杂的调控网络，其中其他应激反应和指数生长期后过程影响phoPR的表达，从而影响Pho调控子反应的强度。
