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首页> 外文期刊>Journal of bacteriology >Evidence for Na+ Influx via the NtpJ Protein of the KtrII K+ Uptake System inEnterococcus hirae
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Evidence for Na+ Influx via the NtpJ Protein of the KtrII K+ Uptake System inEnterococcus hirae

机译:通过平肠肠球菌KtrII K +吸收系统的NtpJ蛋白流入Na +的证据

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The ntpJ gene, a cistron located at the tail end of the vacuolar-type Na+-ATPase (ntp) operon ofEnterococcus hirae, encodes a transporter of the KtrII K+ uptake system. We found that K+ accumulation in the ntpJ-disrupted mutant JEM2 was markedly enhanced by addition of valinomycin at pH 10. Studies of the membrane potential (ΔΨ; inside negative) by 3,3′-dihexyloxacarbocyanine iodide fluorescence revealed that the ΔΨ was hyperpolarized at pH 10 in JEM2; the ΔΨ values of the parent strain ATCC 9790 and JEM2, estimated by determining the equilibrium distribution of K+or Rb+ in the presence of valinomycin, were ?118 and ?160 mV, respectively. ΔΨ generation at pH 10 was accomplished by an electrogenic Na+ efflux via the Na+-ATPase, whose levels in the two strains were quite similar. Na+uptake driven by an artificially imposed ΔΨ (inside negative) was missing in JEM2, suggesting that NtpJ mediates Na+ movement in addition to K+ movement. Finally, the growth of JEM2 arrested in K+-limited high-Na+ medium at pH 10 was restored by addition of valinomycin. These results suggest that NtpJ mediates electrogenic transport of K+ as well as Na+, that it likely mediates K+ and Na+ cotransport, and that Na+ movement via NtpJ is the major Na+ reentry pathway at high pH values.
机译: ntpJ 基因,顺反子,位于肠球菌的液泡型Na + -ATPase( ntp )操纵子的末端hirae ,编码KtrII K + 吸收系统的转运蛋白。我们发现,在pH 10下加入缬霉素可显着增强 ntpJ 破坏的突变体JEM2中的K + 积累。 3,3'-二己基氧杂碳菁碘碘化物的荧光显示JEM2中的ΔΨ在pH 10时超极化。在存在缬氨霉素的情况下,通过确定K + 或Rb + 的平衡分布估算的亲本菌株ATCC 9790和JEM2的ΔΨ值分别为?118和?160 mV,分别。 pH 10时的ΔΨ生成是通过Na + -ATPase的电Na + 外排完成的,这两个菌株中的水平非常相似。 JEM2中缺少由人为施加的Δdriven驱动的Na + 吸收(内部负值),这表明NtpJ除K + 运动。 >运动。最终,通过添加缬氨霉素恢复了在pH 10的K + 限制型高Na + 培养基中滞留的JEM2的生长。这些结果表明,NtpJ介导了K + 和Na + 的电迁移,它可能介导了K + 和Na + 共转运,而通过NtpJ的Na + 运动是高pH值下Na + 的主要折返途径。

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