Key microbial factor involved in regulation of early and late events in tuberculosis infection, and in host-pathogen interactions. Modulates host immunity during early infection. Slows mycobacterial growth during chronic infection in host and during a variety of stress conditions in vitro. Regulates the expression of a large subset of tRNA genes as a means to facilitate adaptation to changing growth environments. In vitro, directs the inhibition of transcription and translation processes in a phosphorylation-dependent manner. Phosphorylates the transcriptional regulator VirS, thereby increasing the affinity of VirS for the mycobacterial monooxygenase (mymA) promoter. In vitro, can also phosphorylate the mycobacterial monooxygenase operon products Rv3083 (MymA), Rv3084 (LipR), Rv3085 and Rv3088. ATP + L-seryl-[protein] = ADP + H(+) + O-phospho-L-seryl-[protein] ATP + L-threonyl-[protein] = ADP + H(+) + O-phospho-L-threonyl-[protein] Forms oligomeric complexes in solution. Probably attached to the cell membrane through interactions mediated by its C-terminal region. May be secreted during infection. Induced during early infection in human macrophages. The C-terminal region exerts intrasteric control that autoregulates kinase activity. Can autophosphorylate the carboxyl terminal region in addition to Thr-179 and Thr-181. Deletion affects cell size and cell wall composition, increases survival during persistent infection in mice, and increases resistance to acidic pH, hypoxia, oxidative and stationary-phase stresses in vitro. Belongs to the protein kinase superfamily. Ser/Thr protein kinase family.