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

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. Na _vBP has roles in motility, chemotaxis, and pH homeostasis at high pH. Reduced motility of bacteria lacking functional Na_vBP was reversed by restoration of the native channel but not by a mutant Na_vBP 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 Na _vBP 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 Na_vBP at high pH supports diverse physiological processes by a combination of direct and indirect effects on the Na⁺ cycle and the chemotaxis system.