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

Masahiro Ito, Haoxing Xu, Arthur A. Guffanti, Yi Wei, Lior Zvi, David E. Clapham, Terry A. Krulwich

Research output: Contribution to journalArticlepeer-review

86 Scopus citations

Abstract

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 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 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 NavBP at high pH supports diverse physiological processes by a combination of direct and indirect effects on the Na+ cycle and the chemotaxis system.

Original languageEnglish
Pages (from-to)10566-10571
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume101
Issue number29
DOIs
StatePublished - 20 Jul 2004

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