M. tuberculosis phoP-phoR system controls a variety of functions including stress response, respiratory metabolism, secretion of the major T-cell antigen ESAT-6, and synthesis of pathogenic lipids. Thus, a phoP disruption mutant of M. tuberculosis is significantly growth attenuated in animal models. However, the exact role of PhoP in intracellular growth of the bacilli or the basis for growth attenuation of the phoP mutant in macrophages and mice remains unknown. Our work showing PhoP phosphorylation, DNA-protein and protein-protein interactions by the regulator represent the most original contributions to our understanding on how this system impacts different aspects of M. tuberculosis physiology.

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