Kawano M, Igarashi K, Kakinuma Y
Faculty of Pharmaceutical Sciences, Chiba University, Inage-ku, Chiba 263-8522, Japan.
J Bacteriol. 1998 Sep;180(18):4942-5. doi: 10.1128/JB.180.18.4942-4945.1998.
Enterococcus hirae ATCC 9790 grew well in Na+-deficient, low-K+ medium, but growth was inhibited by carbonylcyanide m-chlorophenylhydrazone (CCCP). Growth inhibition and decrease of cellular K+ levels in the presence of CCCP were relieved by the addition of Na+ and a high concentration of K+. In contrast, in the mutant defective in Na+-ATPase or the NtpJ component of the KtrII K+ uptake system, CCCP-induced growth inhibition was rescued by a high concentration of K+ but not of Na+. These transporters are thus indispensable for homeostatis of K+ and Na+ at low proton potential.
平肠球菌ATCC 9790在缺钠、低钾培养基中生长良好,但生长受到羰基氰化物间氯苯腙(CCCP)的抑制。添加Na⁺和高浓度的K⁺可缓解CCCP存在时的生长抑制和细胞K⁺水平降低。相比之下,在Na⁺-ATP酶或KtrII K⁺摄取系统的NtpJ组分有缺陷的突变体中,高浓度的K⁺而非Na⁺可挽救CCCP诱导的生长抑制。因此,这些转运蛋白对于低质子势下K⁺和Na⁺的稳态是不可或缺的。