Abstract
The ε subunit of F(o) F(1) -ATPase/synthase (F(o) F(1) ) plays a crucial role in regulating F(o) F(1) activity. To understand the physiological significance of the ε subunit-mediated regulation of F(o) F(1) in Bacillus subtilis, we constructed and characterized a mutant harboring a deletion in the C-terminal regulatory domain of the ε subunit (ε(∆C) ). Analyses using inverted membrane vesicles revealed that the ε(∆C) mutation decreased ATPase activity and the ATP-dependent H(+) -pumping activity of F(o) F(1) . To enhance the effects of ε(∆C) mutation, this mutation was introduced into a ∆rrn8 strain harboring only two of the 10 rrn (rRNA) operons (∆rrn8 ε(∆C) mutant strain). Interestingly, growth of the ∆rrn8 ε(∆C) mutant stalled at late-exponential phase. During the stalled growth phase, the membrane potential of the ∆rrn8 ε(∆C) mutant cells was significantly reduced, which led to a decrease in the cellular level of 70S ribosomes. The growth stalling was suppressed by adding glucose into the culture medium. Our findings suggest that the C-terminal region of the ε subunit is important for alleviating the temporal reduction in the membrane potential, by enhancing the ATP-dependent H(+) -pumping activity of F(o) F(1) .