1887

Abstract

Mg has been shown to be an important signal controlling gene regulation via the PhoPQ two-component regulatory system for a range of Gram-negative bacteria, including and . The magnesium ion transporter MgtB is part of the complex PhoPQ regulon, being upregulated in response to low Mg. Despite the presence of other Mg transport systems in , inactivation of had a significant effect on the ability of the bacteria to scavenge this crucial ion. Whereas inactivation of PhoPQ is reported to adversely affect intracellular survival, we show that and Δ mutants survived equally as well as the respective parent strain within macrophages, although they were more sensitive to killing in the model of infection. Surprisingly, despite MgtB being only one member of the Mg stimulon and PhoPQ controlling the expression levels of a range of genes including , the Δ mutants were more highly attenuated than the equivalent Δ mutants in mouse models of infection. MgtB may be a suitable target for development of novel antimicrobials, and investigation of its role may help elucidate the contribution of this component of the PhoPQ regulon to pathogenesis.

Funding
This study was supported by the:
  • UK Ministry of Defence
  • BBSRC (Award BB/D52336X/1)
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2014-12-01
2024-04-18
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