A new player at the flagellar motor: FliL controls both motor output and bias.
A new player at the flagellar motor: FliL controls both motor output and bias.
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DOI：
10.1128/mbio.02367-14
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发表时间：
2015-02-24
期刊：
影响因子：
6.4
通讯作者：
Harshey RM
中科院分区：
文献类型：
--
作者：
Partridge JD;Nieto V;Harshey RM
细菌鞭毛由一个双向旋转马达驱动，该马达推动细菌在液体中游动或在表面上游动。虽然鞭毛的主要结构和调节组分的功能是已知的，但高度保守的FliL蛋白的功能是未知的。在沙门氏菌和大肠杆菌中，FliL的缺失导致游动的小缺陷，但完全消除了群集。在这里，我们跟踪了这些细菌的单个马达，发现缺乏FliL会降低它们的速度和开关频率。我们表明，FliL强烈相互作用，与MS环蛋白FliF，并与定子蛋白MotA和MotB和转子开关蛋白FliG弱。这些和其他实验表明，FliL通过招募或稳定定子或通过提高其效率来增加电机输出，并在更高的电机负载下额外地产生扭矩。FliL增加的扭矩解释了为什么这种蛋白质对于在琼脂表面上聚集是必不可少的，预期会增加对细菌运动的抵抗力。FliL是一种高度保守的细菌鞭毛蛋白，其缺失导致各种运动缺陷，范围从一些细菌物种中的游泳的中度至完全抑制，其他细菌物种中的群集抑制，大肠杆菌和沙门氏菌中群集期间破坏鞭毛杆的结构缺陷，以及新月柄杆菌中游泳者向柄细胞发育过渡期间未能射出鞭毛丝。尽管有这些表型，FliL的特定功能仍然难以捉摸。在这里，我们确定了FliL在沙门氏菌和大肠杆菌马达中的核心作用，在那里它与转子和定子蛋白相互作用，增加马达输出，并有助于马达的正常旋转偏置。
The bacterial flagellum is driven by a bidirectional rotary motor, which propels bacteria to swim through liquids or swarm over surfaces. While the functions of the major structural and regulatory components of the flagellum are known, the function of the well-conserved FliL protein is not. In Salmonella and Escherichia coli, the absence of FliL leads to a small defect in swimming but complete elimination of swarming. Here, we tracked single motors of these bacteria and found that absence of FliL decreases their speed as well as switching frequency. We demonstrate that FliL interacts strongly with itself, with the MS ring protein FliF, and with the stator proteins MotA and MotB and weakly with the rotor switch protein FliG. These and other experiments show that FliL increases motor output either by recruiting or stabilizing the stators or by increasing their efficiency and contributes additionally to torque generation at higher motor loads. The increased torque enabled by FliL explains why this protein is essential for swarming on an agar surface expected to offer increased resistance to bacterial movement. FliL is a well-conserved bacterial flagellar protein whose absence leads to a variety of motility defects, ranging from moderate to complete inhibition of swimming in some bacterial species, inhibition of swarming in others, structural defects that break the flagellar rod during swarming in E. coli and Salmonella, and failure to eject the flagellar filament during the developmental transition of a swimmer to a stalk cell in Caulobacter crescentus. Despite these many phenotypes, a specific function for FliL has remained elusive. Here, we established a central role for FliL at the Salmonella and E. coli motors, where it interacts with both rotor and stator proteins, increases motor output, and contributes to the normal rotational bias of the motor.