Antitoxin MqsA helps mediate the bacterial general stress response.

Antitoxin MqsA helps mediate the bacterial general stress response.
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DOI:
10.1038/nchembio.560
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发表时间:
2011-06
影响因子:
14.8
通讯作者:
Wood, Thomas K.
Wood, Thomas K.
中科院分区:
生物学1区
文献类型:
--
作者:
Wang, Xiaoxue;Kim, Younghoon;Hong, Seok Hoon;Ma, Qun;Brown, Breann L.;Pu, Mingming;Tarone, Aaron M.;Benedik, Michael J.;Peti, Wolfgang;Page, Rebecca;Wood, Thomas K.

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虽然人们普遍认为细菌通过全球网络对环境压力做出反应,但对压力传递到细胞内部的机制知之甚少。在这里,我们表明,神秘的毒素/抗毒素系统在介导的环境应激反应中起着至关重要的作用。具体而言,抗毒素MqsA抑制rpoS,其编码应激的主调节因子。MqsA对rpoS的抑制降低了内部信使3,5-环二鸟苷酸的浓度,导致运动性增加和生物膜形成减少。此外,MqsA对rpoS的抑制通过过氧化氢酶活性降低氧化应激抗性。在氧化应激时,MqsA被Lon蛋白酶快速降解,导致rpoS的诱导。因此,我们表明,外部压力改变了毒素/抗毒素系统控制的基因调控,这样,在应力过程中的抗毒素的降解导致从反张状态(高运动性)的生物膜状态(低运动性)的开关。
Although it is well-recognized that bacteria respond to environmental stress via global networks, the mechanism by which stress is relayed to the interior of the cell is poorly understood. Here we show that enigmatic toxin/antitoxin systems play a vital role in mediating the environmental stress response. Specifically, the antitoxin MqsA represses rpoS, which encodes the master regulator of stress. Repression of rpoS by MqsA reduces the concentration of the internal messenger 3,5-cyclic diguanylic acid, leading to increased motility and decreased biofilm formation. Furthermore, the repression of rpoS by MqsA decreases oxidative stress resistance via catalase activity. Upon oxidative stress, MqsA is rapidly degraded by Lon protease resulting in induction of rpoS. Hence, we show that external stress alters gene regulation controlled by toxin/antitoxin systems, such that the degradation of antitoxins during stress leads to a switch from the planktonic state (high motility) to the biofilm state (low motility).
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