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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