Role of cyclic di AMP in mycobacterial physiology and virulence
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Abstract
Mycobacterium tuberculosis (M. tb.), one of the three most infectious pathogens
newlineworldwide goes through different stages in their life cycle. M. tb. resides within human
newlinemacrophages in latent stage for long periods of time before they get activated and infect the host. M. tb. adapts to these conditions utilizing various signaling molecules and pathways. M. tb. overcomes the immune response mounted by macrophages during their
newlinelatent stage. Many of the agents which are produced as part of immune response like
newlinereactive nitrogen and oxygen species cause different damages to bacterial DNA. Lot of work has been done to understand the different DNA repair pathways present in mycobacterium
newlinebut very little is known about the signaling of damage and repair. Mycobacterium has a DisA
newlinehomolog (Rv3586 in H37Rv strain) and it appears to be a good candidate to signal DNA damage. DisA exists in an operon with RadA (Rv3585) and it is provocative to think that DisA and RadA act together at DNA breaks.
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