期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：2004
卷号：101
期号：29
页码：10566-10571
DOI：10.1073/pnas.0402692101
语种：English
出版社：The National Academy of Sciences of the United States of America
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.
