Mycobacterium tuberculosis Requires Phosphate-Responsive Gene Regulation To Resist Host Immunity

Anna D. Tischler, Rachel L. Leistikow, Meghan A. Kirksey, Martin I. Voskuil, John D. McKinney
  • Infection and Immunity, November 2012, ASM Journals
  • DOI: 10.1128/iai.01136-12

Mycobacterium tuberculosis PstA1 Counters Host Immunity

What is it about?

In phosphate-poor environments, bacteria require the high-affinity phosphate-specific transport (Pst) system for uptake of inorganic phosphate. We demonstrate that the M. tuberculosis Pst system controls gene expression in response to high levels of external phosphate by repressing activity of the two-component signal transduction system SenX3-RegX3 and show that this regulatory functions is critical for surviving host adaptive immune responses.

Why is it important?

Previous studies established that M. tuberculosis requires the Pst system for replication in macrophages or in the lungs of mice, which was interpreted as evidence that the bacteria are phosphate-starved in host tissues. Our data suggest that M. tuberculosis sometimes requires the Pst system to switch off expression of phosphate-starvation responsive genes. We have also identified a signal transduction pathway that could be targeted by drugs to make the bacteria susceptible to host immunity.

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The following have contributed to this page: Anna Tischler and Dr Martin I Voskuil