Magnesium uptake by CorA is essential for viability of the gastric pathogen Helicobacter pylori.
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.
Pfeiffer
Jens
J
Department of Medical Microbiology and Hygiene, Institute of Medical Microbiology and Hygiene, University Hospital of Freiburg, D-79104 Freiburg, Germany.
Guhl
Johannes
J
Waidner
Barbara
B
Kist
Manfred
M
Bereswill
Stefan
S
D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D027682:Cation Transport Proteins / Q000235:genetics / Q000378:metabolism*; D003035:Cobalt / Q000378:metabolism; D004926:Escherichia coli / Q000378:metabolism; D016480:Helicobacter pylori / Q000235:genetics / Q000254:growth & development / Q000302:isolation & purification / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism*; D009532:Nickel / Q000378:metabolism; D013270:Stomach / Q000382:microbiology
D001426:Bacterial Proteins; D027682:Cation Transport Proteins; D003035:Cobalt; D009532:Nickel; D008274:Magnesium