PDF(Pubmed)
Abstract：
The universally conserved YchF/Ola1 ATPases regulate stress response pathways in prokaryotes and eukaryotes. Deletion of YchF/Ola1 leads to increased resistance against environmental stressors, such as reactive oxygen species, while their upregulation is associated with tumorigenesis in humans. The current study shows that in E. coli, the absence of YchF stimulates the synthesis of the alternative sigma factor RpoS by a transcription-independent mechanism. Elevated levels of RpoS then enhance the transcription of major stress-responsive genes. In addition, the deletion of ychF increases the levels of polyphosphate kinase, which in turn boosts the production of the evolutionary conserved and ancient chemical chaperone polyphosphate. This potentially provides a unifying concept for the increased stress resistance in bacteria and eukaryotes upon YchF/Ola1 deletion. Intriguingly, the simultaneous deletion of ychF and the polyphosphate-degrading enzyme exopolyphosphatase causes synthetic lethality in E. coli, demonstrating that polyphosphate production needs to be fine-tuned to prevent toxicity.
摘要：
普遍保守的YchF/Ola1ATPases调节原核生物和真核生物的应激反应途径。删除YchF/Ola1会导致对环境压力源的抵抗力增加，比如活性氧，而它们的上调与人类的肿瘤发生有关。目前的研究表明，在大肠杆菌中，YchF的缺失通过不依赖转录的机制刺激替代sigma因子RpoS的合成。升高的RpoS水平则增强了主要应激反应基因的转录。此外,YchF的缺失增加了多磷酸激酶的水平，这反过来又促进了进化保守和古老的化学伴侣多磷酸盐的产生。这可能为YchF/Ola1缺失后细菌和真核生物的胁迫抗性增加提供统一的概念。有趣的是，YchF和多磷酸盐降解酶外聚磷酸酶的同时缺失导致大肠杆菌的合成致死性，证明聚磷酸盐的生产需要进行微调以防止毒性。
