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The voltage-gated Na+ channel NaVBP has a role in motility, chemotaxis, and pH homeostasis of an alkaliphilic Bacillus

机译:电压门控的Na +通道NaVBP在嗜碱芽孢杆菌的运动性,趋化性和pH稳态中起作用

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摘要

The prokaryotic voltage-gated Na+ channel, NaChBac, is one of a growing channel superfamily of unknown function. Here we show that NaVBP, the NaChBac homologue encoded by ncbA in alkaliphilic Bacillus pseudofirmus OF4, is a voltage-gated Na+ channel potentiated by alkaline pH. NaVBP has roles in motility, chemotaxis, and pH homeostasis at high pH. Reduced motility of bacteria lacking functional NaVBP was reversed by restoration of the native channel but not by a mutant NaVBP engineered to be Ca2+-selective. Motile ncbA mutant cells and wild-type cells treated with a channel inhibitor exhibited behavior opposite to the wild type in response to chemoeffectors. Mutants lacking functional NaVBP were also defective in pH homeostasis in response to a sudden alkaline shift in external pH under conditions in which cytoplasmic [Na+] is limiting for this crucial process. The defect was exacerbated by mutation of motPS, the motility channel genes. We hypothesize that activation of NaVBP at high pH supports diverse physiological processes by a combination of direct and indirect effects on the Na+ cycle and the chemotaxis system.
机译:电压门控的Na +通道NaChBac,是功能未知的生长通道超家族之一。在这里,我们显示NaVBP,由ncbA编码在嗜碱芽孢杆菌OF4中的NaChBac同源物,是由碱性pH增强的电压门控Na +通道。 NaVBP在高pH下具有运动性,趋化性和pH稳态。缺乏功能性NaVBP的细菌运动力的降低可通过恢复天然通道来逆转,但不能通过设计为Ca2 +选择性的突变NaVBP来逆转。用通道抑制剂处理的可动性ncbA突变细胞和野生型细胞对化学效应物的反应与野生型相反。在细胞质[Na +]限制了这一关键过程的条件下,缺乏功能性NaVBP的突变体在pH稳态方面也存在缺陷,这是由于外部pH的突然碱性变化引起的。动力通道基因motPS突变加剧了该缺陷。我们假设在高pH值下NaVBP的激活通过对Na +循环和趋化性系统的直接和间接影响的组合支持多种生理过程。

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