Magnesium uptake by CorA is essential for viability of the gastric pathogen Helicobacter pylori

Infect Immun. 2002 Jul;70(7):3930-4. doi: 10.1128/IAI.70.7.3930-3934.2002.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • Cation Transport Proteins / genetics
  • Cation Transport Proteins / metabolism*
  • Cobalt / metabolism
  • Escherichia coli / metabolism
  • Helicobacter pylori / genetics
  • Helicobacter pylori / growth & development
  • Helicobacter pylori / isolation & purification
  • Helicobacter pylori / metabolism*
  • Magnesium / metabolism*
  • Nickel / metabolism
  • Stomach / microbiology

Substances

  • Bacterial Proteins
  • Cation Transport Proteins
  • Cobalt
  • Nickel
  • Magnesium