Pfeiffer Jens, Guhl Johannes, Waidner Barbara, Kist Manfred, Bereswill Stefan
Department of Medical Microbiology and Hygiene, Institute of Medical Microbiology and Hygiene, University Hospital of Freiburg, D-79104 Freiburg, Germany.
Infect Immun. 2002 Jul;70(7):3930-4. doi: 10.1128/IAI.70.7.3930-3934.2002.
We show here that Mg(2+) acquisition by CorA is essential for Helicobacter pylori in vitro, as corA mutants did not grow in media without Mg(2+) supplementation. Complementation analysis performed with an Escherichia coli corA mutant revealed that H. pylori CorA transports nickel and cobalt in addition to Mg(2+). However, Mg(2+) is the dominant CorA substrate, as the corA mutation affected neither cobalt and nickel resistance nor nickel induction of urease in H. pylori. The drastic Mg(2+) requirement (20 mM) of H. pylori corA mutants indicates that CorA plays a key role in the adaptation to the low-Mg(2+) conditions predominant in the gastric environment.
我们在此表明,CorA对镁离子(Mg²⁺)的摄取对幽门螺杆菌在体外生长至关重要,因为corA突变体在未补充Mg²⁺的培养基中无法生长。对大肠杆菌corA突变体进行的互补分析表明,幽门螺杆菌CorA除了转运Mg²⁺外,还转运镍和钴。然而,Mg²⁺是主要的CorA底物,因为corA突变既不影响幽门螺杆菌对钴和镍的抗性,也不影响镍对脲酶的诱导。幽门螺杆菌corA突变体对Mg²⁺的严格需求(20 mM)表明,CorA在适应胃环境中占主导地位的低Mg²⁺条件方面发挥着关键作用。