Member of the two-component regulatory system DevR/DevS (also called DosR/DosS) involved in onset of the dormancy response (PubMed:15033981). Regulates an approximately 48-member regulon (PubMed:12953092, PubMed:11416222, PubMed:15033981, PubMed:18400743). When phosphorylated binds and activates the promoter of DevR regulon genes in response to hypoxia (PubMed:18359816, PubMed:21764934, PubMed:28977726). The presence of target DNA increases stability of phospho-DevR in vitro (PubMed:28977726). Activates its own transcription under hypoxic but not aerobic conditions, probably binds as a dimer to tandem binding sites within the devR and hspX promoters (PubMed:18359816). Accepts a phosphate group from DevS (DosS) and from DosT (PubMed:15033981, PubMed:15073296, PubMed:21764934, PubMed:28977726). Does not regulate transcription of dosT (PubMed:19487478). Homodimer (PubMed:18353359). Interacts with NarL (PubMed:25659431). (Microbial infection) In human monocytes after in vitro infection (PubMed:10970762). A member of the dormancy regulon. Moderately expressed under aerobic conditions, it is strongly induced in response to reduced oxygen tension (hypoxia), low levels of nitric oxide (NO) and carbon monoxide (CO) (PubMed:11416222, PubMed:12953092, PubMed:17609369, PubMed:18474359, PubMed:18400743). It is hoped that this regulon will give insight into the latent, or dormant phase of infection. Expression under hypoxic conditions, but not aerobically, is autoregulated. Member of the Rv3134c-devR-devS operon (PubMed:10970762). Phosphorylated on Asp-54 by both DevS (DosS) and DosT (PubMed:15033981, PubMed:15073296, PubMed:21764934). Phosphorylated on Thr-198 and Thr-205 by PknH, which enhances DevR dimerization (PubMed:20630871). Aspartate phosphorylation and threonine phosphorylation cooperatively enhance DevR binding to DNA (PubMed:20630871). Strains deleted for this gene show hypervirulence upon intravenous inoculation in the mouse and DBA/2 model (PubMed:12595424). However contradictory results were shown for using a devR/devS deletion strain in rabbits, guinea pigs and C57BL/6 mice (PubMed:19103767). All studies agree that deletion strains fail to induce the dormancy regulon genes in response to hypoxia, NO, and CO (PubMed:11416222, PubMed:12694625, PubMed:18474359, PubMed:18400743, PubMed:19487478). Deletion has no effect on expression of dosT (PubMed:19487478). The dev nomenclature derives from the increased expression (differentially expressed in virulent strain, dev) of these genes in virulent H37Rv versus avirulent H37Ra. The dos nomenclature derives from experiments in M.bovis showing the same genes are essential for dormancy survival (dos).