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( Mtb ) produces inflections in the host signaling networks to create a favorable milieu for survival. The virulent  Mtb  strain,  Rv  caused double strand breaks (DSBs), whereas the non-virulent  Ra  strain triggered single-stranded DNA generation. The effectors secreted by SecA2 pathway were essential and adequate for the genesis of DSBs. Accumulation of DSBs mediated through  Rv  activates ATM-Chk2 pathway of DNA damage response (DDR) signaling, resulting in altered cell cycle. Instead of the classical ATM-Chk2 DDR,  Mtb  gains survival advantage through ATM-Akt signaling cascade. Notably, in vivo infection with  Mtb  led to sustained DSBs and ATM activation during chronic phase of tuberculosis. Addition of ATM inhibitor enhances isoniazid mediated  Mtb  clearance in macrophages as well as in murine infection model, suggesting its utility for host directed adjunct therapy. Collectively, data suggests that DSBs inflicted by SecA2 secretome of  Mtb  provides survival niche through activation of ATM kinase.

Mycobacterium tuberculosis exploits host ATM kinase for survival advantage through SecA2 secretome