Bacterial eukaryotic-like serine threonine kinases (eSTKs) and serine threonine phosphatases (eSTPs) have emerged as important signaling elements that are indispensable for pathogenesis. Differing considerably from their histidine kinase counterparts, few eSTK genes are encoded within the average bacterial genome, and their targets are pleiotropic in nature instead of exclusive. The growing list of important eSTK/P substrates includes proteins involved in translation, cell division, peptidoglycan synthesis, antibiotic tolerance, resistance to innate immunity and control of virulence factors. Recently it has come to light that eSTK/Ps also directly modulate transcriptional machinery in many microbial pathogens. This novel form of regulation is now emerging as an additional means by which bacteria can alter their transcriptomes in response to host-specific environmental stimuli. Here we focus on the ability of eSTKs and eSTPs in Gram-positive bacterial pathogens to directly modulate transcription, the known mechanistic outcomes of these modifications, and their roles as an added layer of complexity in controlling targeted RNA synthesis to enhance virulence potential.
Keywords: OCS, one-component signaling; PASTA, penicillin-binding protein and Ser/Thr kinase associated; PPM, protein phosphatase metal binding; PTM, posttranslational modification; REC, receiver; ROS, reactive oxygen species; TCS, two-component signaling; bacteria; eSTK, eukaryotic-like serine-threonine kinase; eSTP, eukaryotic-like serine-threonine phosphatase; infection; phosphorylation; serine threonine kinase; serine threonine phosphatase; transcription; wHTH, winged helix-turn-helix.