Mycobacterium tuberculosis is the causative agent of tuberculosis. M. tuberculosis can survive in a dormant state within
the granuloma, avoiding the host-mounting immune attack. M. tuberculosis bacilli in this state show increased tolerance
to antibiotics and stress conditions, and thus the transition of M. tuberculosis to the nonreplicating dormant state acts as
an obstacle to tuberculosis treatment. M. tuberculosis in the granuloma encounters hostile environments such as hypoxia,
nitric oxide, reactive oxygen species, low pH, and nutrient deprivation, etc., which are expected to inhibit respiration of M.
tuberculosis. To adapt to and survive in respiration-inhibitory conditions, it is required for M. tuberculosis to reprogram its
metabolism and physiology. In order to get clues to the mechanism underlying the entry of M. tuberculosis to the dormant
state, it is important to understand the mycobacterial regulatory systems that are involved in the regulation of gene expression
in response to respiration inhibition. In this review, we briefly summarize the information regarding the regulatory
systems implicated in upregulation of gene expression in mycobacteria exposed to respiration-inhibitory conditions. The
regulatory systems covered in this review encompass the DosSR (DevSR) two-component system, SigF partner switching
system, MprBA-SigE-SigB signaling pathway, cAMP receptor protein, and stringent response.