RpoS是在许多γ变形菌中诱导一般应激反应所需的替代σ因子。RpoS水平和活性的严格调节是细菌在胁迫下生长和存活所必需的。在大肠杆菌中,由于翻译增加和降解减少,各种应力导致更高水平的RpoS。在非压力条件下,Rpos是不稳定的,因为衔接蛋白RssB将RpoS传递给ClpXP蛋白酶。通过抗衔接子隔离RssB,可以在应激过程中防止RpoS降解,每个都是响应特定的应力而诱导的。这里,我们研究了在细胞从应激中恢复过程中RpoS的稳定性是如何逆转的。我们发现,从磷酸盐饥饿中恢复后,RpoS降解迅速恢复,碳饥饿,当从固定阶段过渡到指数阶段时。这个过程部分是由抗适配器IraP介导的,已知通过衔接子RssB的螯合在磷酸盐饥饿期间促进RpoS稳定。从磷酸盐饥饿中的快速恢复取决于反馈回路,其中rssB的RpoS转录,编码衔接蛋白,起着关键作用。Crl,RpoS的激活剂,特异性结合并稳定RNA聚合酶和RpoS之间的复合物,也需要反馈回路有效地运行,强调Crl在恢复RpoS基础水平中的关键作用。
RpoS is an alternative sigma factor needed for the induction of the general stress response in many gammaproteobacteria. Tight regulation of RpoS levels and activity is required for bacterial growth and survival under stress. In Escherichia coli, various stresses lead to higher levels of RpoS due to increased translation and decreased degradation. During non-stress conditions, RpoS is unstable, because the
adaptor protein RssB delivers RpoS to the ClpXP protease. RpoS degradation is prevented during stress by the sequestration of RssB by anti-adaptors, each of which is induced in response to specific stresses. Here, we examined how the stabilization of RpoS is reversed during recovery of the cell from stress. We found that RpoS degradation quickly resumes after recovery from phosphate starvation, carbon starvation, and when transitioning from stationary phase back to exponential phase. This process is in part mediated by the anti-
adaptor IraP, known to promote RpoS stabilization during phosphate starvation via the sequestration of
adaptor RssB. The rapid recovery from phosphate starvation is dependent upon a feedback loop in which RpoS transcription of rssB, encoding the
adaptor protein, plays a critical role. Crl, an activator of RpoS that specifically binds to and stabilizes the complex between the RNA polymerase and RpoS, is also required for the feedback loop to function efficiently, highlighting a critical role for Crl in restoring RpoS basal levels.