Abstract
In alkaliphilic Bacillus, Na+-dependent pH homeostasis involves antiport activities as well as Na+ re-entry routes. MotPS that are homologous to MotAB are required for the Na+-dependent motility of alkaliphilic B. pseudofirmus OF4. Purified and reconstituted MotPS support amiloride analogue-sensitive Na+ flux. Mutants lacking functional MotPS display no deficit in pH homeostasis in pH shift experiments conducted with sub-optimal added [Na+] in the absence of solutes whose uptake is coupled to Na+ re-entry. By contrast, a role was evident for the recently described NaChBac (voltage-dependent) Na+ channel at sub-optimal [Na+]. NaChBac mutants exhibit a significant loss of pH homeostasis capacity.
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