The voltage-gated Na+ channel NavBP has a role in motility, chemotaxis, and pH homeostasis of an alkaliphilic Bacillus
The voltage-gated Na+ channel NavBP has a role in motility, chemotaxis, and pH homeostasis of an alkaliphilic Bacillus
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DOI：
10.1073/pnas.0402692101
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发表时间：
2004-07-20
影响因子：
11.1
通讯作者：
Krulwich, TA
中科院分区：
文献类型：
--
作者：
Ito, M;Xu, HX;Krulwich, TA
原核细胞电压门控Na+通道（NaChBac）是一个功能未知的通道超家族。在这里，我们表明，NaVBP，由ncbA编码的NaChBac同系物在嗜碱芽孢杆菌pseudofirmus OF 4，是一个电压门控的Na+通道增强碱性pH值。NaVBP的作用，在运动，趋化性，和pH值在高pH值的稳态。减少缺乏功能NaVBP的细菌的运动被逆转的恢复本机通道，但不是由突变体NaVBP工程改造为Ca 7 +-选择性。运动ncbA突变体细胞和野生型细胞与通道抑制剂处理表现出相反的野生型响应于化学效应的行为。缺乏功能性NaVBP的突变体也有缺陷的pH值的稳态响应于突然的碱性转变外部pH值的条件下，细胞质[Na+]是限制这一关键过程。运动通道基因motPS的突变加剧了这种缺陷。我们假设NaVBP在高pH值下的激活通过对Na+循环和趋化系统的直接和间接影响的结合来支持不同的生理过程。
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 Ca7+-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.