Epsilon subunit, an endogenous inhibitor of bacterial F(1)-ATPase, also inhibits F(0)F(1)-ATPase.
Epsilon subunit, an endogenous inhibitor of bacterial F(1)-ATPase, also inhibits F(0)F(1)-ATPase.
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Epsilon 亚基是细菌 F(1)-ATP 酶的内源性抑制剂，也能抑制 F(0)F(1)-ATP 酶。
DOI：
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发表时间：
1999
影响因子：
4.8
通讯作者：
M. Yoshida
中科院分区：
文献类型：
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作者：
Y. Kato;D. Bald;M. Koike;K. Motohashi;T. Hisabori;M. Yoshida
自从Sternweis和Smith（Sternweis，P.C.，和Smith，J. B.（1980）Biochemistry 19，526-531），细菌F（1）-ATP酶的内源性抑制剂α-ATP酶亚基长期以来被认为不抑制全酶F（0）F（1）-ATP酶的活性。然而，我们在这里报告，在F（0）F（1）-ATP酶中，α-ATP酶亚基发挥抑制作用。我们制备了嗜热芽孢杆菌PS3 F（0）F（1）-ATP酶的C-末端半截短的Δ C亚基（Δ C）和含有Δ C的重构的F（1）-和F（0）F（1）-ATP酶（Δ C）。与含有完整ATP酶的F（1）-和F（0）F（1）-ATP酶相比，含有ATP酶（DeltaC）的ATP酶表现出不受抑制的活性;在低ATP浓度下，ATP水解速率高几倍，在高ATP浓度下，ATP水解开始而没有初始滞后。含有Δ C的F（0）F（1）-ATPase能够在ATP驱动下泵吸H（+）。在低ATP浓度下，泵送的时间过程比含有完整ATP的F（0）F（1）-ATP酶快。因此，与非抑制性Δ C（DeltaC）突变体的比较揭示了完整Δ C亚基在F（0）F（1）-ATP酶中的抑制作用。
Since the report by Sternweis and Smith (Sternweis, P. C., and Smith, J. B. (1980) Biochemistry 19, 526-531), the epsilon subunit, an endogenous inhibitor of bacterial F(1)-ATPase, has long been thought not to inhibit activity of the holo-enzyme, F(0)F(1)-ATPase. However, we report here that the epsilon subunit is exerting inhibition in F(0)F(1)-ATPase. We prepared a C-terminal half-truncated epsilon subunit (epsilon(DeltaC)) of the thermophilic Bacillus PS3 F(0)F(1)-ATPase and reconstituted F(1)- and F(0)F(1)-ATPase containing epsilon(DeltaC). Compared with F(1)- and F(0)F(1)-ATPase containing intact epsilon, those containing epsilon(DeltaC) showed uninhibited activity; severalfold higher rate of ATP hydrolysis at low ATP concentration and the start of ATP hydrolysis without an initial lag at high ATP concentration. The F(0)F(1)-ATPase containing epsilon(DeltaC) was capable of ATP-driven H(+) pumping. The time-course of pumping at low ATP concentration was faster than that by the F(0)F(1)-ATPase containing intact epsilon. Thus, the comparison with noninhibitory epsilon(DeltaC) mutant shed light on the inhibitory role of the intact epsilon subunit in F(0)F(1)-ATPase.