YihE kinase is a central regulator of programmed cell death in bacteria.
YihE kinase is a central regulator of programmed cell death in bacteria.
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DOI：
10.1016/j.celrep.2013.01.026
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发表时间：
2013-02-21
期刊：
影响因子：
8.8
通讯作者：
Zhao X
中科院分区：
文献类型：
--
作者：
Dorsey-Oresto A;Lu T;Mosel M;Wang X;Salz T;Drlica K;Zhao X
细菌中的应激介导的程序性细胞死亡(PCD)最近引起了人们的关注，主要是因为它为控制病原体提供了新的可能性。如何调控细菌中的PCD，以避免因短暂、适度的压力而导致种群灭绝，仍然是一个核心问题。我们报道，一和蛋白激酶是一种关键的调节因子，通过拮抗MazEF毒素-抗毒素模块来保护大肠杆菌免受抗菌素和环境应激的影响。一和与ROS级联有关，一和的缺乏刺激了应激诱导的PCD，即使在应激消散后也是如此。伊和部分受CPX包膜应激反应系统的调控，该系统与MazF毒素和超氧化物歧化一起，具有保护和破坏作用，帮助细菌在应对压力时做出生死攸关的决定。义和可能在胁迫反应的早期就限制了自给自足的ROS产生和PCD。抑制一和可能为提高抗菌药物的杀伤力和降低毒力提供了新的途径。
Stress-mediated programmed cell death (PCD) in bacteria has recently attracted attention, largely because it raises novel possibilities for controlling pathogens. How PCD in bacteria is regulated to avoid population extinction from transient, moderate stress remains a central question. We report that the YihE protein kinase is a key regulator that protects Escherichia coli from antimicrobial and environmental stressors by antagonizing the MazEF toxin-antitoxin module. YihE was linked to a reactive oxygen species (ROS) cascade, and a deficiency of yihE stimulated stress-induced PCD even after stress dissipated. YihE was partially regulated by the Cpx envelope stress-response system, which, along with MazF toxin and superoxide, has both protective and destructive roles that help bacteria make a live-or-die decision in response to stress. YihE probably acts early in the stress response to limit self-sustaining ROS production and PCD. Inhibition of YihE may provide a new way to enhance antimicrobial lethality and attenuate virulence.