Second Messenger-Mediated Adjustment of Bacterial Swimming Velocity

Second Messenger-Mediated Adjustment of Bacterial Swimming Velocity
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DOI:
10.1016/j.cell.2010.01.018
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发表时间:
2010-04-01
期刊:
影响因子:
64.5
通讯作者:
Jenal, Urs
Jenal, Urs
中科院分区:
生物学1区
文献类型:
--
作者:
Boehm, Alex;Kaiser, Matthias;Jenal, Urs

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细菌通过旋转的鞭毛游泳,鞭毛由跨越膜的马达复合体的离子内流提供动力。大肠杆菌和相关物种利用一种化学感觉和信号转导机制,控制鞭毛旋转的方向,并允许它们在化学梯度中导航。在这里,我们证明了大肠杆菌也可以在分子刹车(YcgR)的帮助下微调其游泳速度,分子刹车在与核苷酸第二信使环双GMP结合时,与马达蛋白MoTA相互作用,以抑制鞭毛马达的输出。游泳速度是由至少五种信号蛋白的协同作用控制的,这些信号蛋白调节细胞内环二核苷酸的浓度。这一网络的激活和由此产生的减速与营养物质的枯竭相吻合,可能代表着对饥饿的适应。这些实验表明,细菌可以调节鞭毛马达的输出,从而对环境线索做出反应,从而调节游泳速度。
Bacteria swim by means of rotating flagella that are powered by ion influx through membrane-spanning motor complexes. Escherichia coli and related species harness a chemosensory and signal transduction machinery that governs the direction of flagellar rotation and allows them to navigate in chemical gradients. Here, we show that Escherichia coli can also fine-tune its swimming speed with the help of a molecular brake (YcgR) that, upon binding of the nucleotide second messenger cyclic di-GMP, interacts with the motor protein MotA to curb flagellar motor output. Swimming velocity is controlled by the synergistic action of at least five signaling proteins that adjust the cellular concentration of cyclic di-GMP. Activation of this network and the resulting deceleration coincide with nutrient depletion and might represent an adaptation to starvation. These experiments demonstrate that bacteria can modulate flagellar motor output and thus swimming velocity in response to environmental cues.