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Background  Molecular programs employed by  Mycobacterium tuberculosis  ( Mtb ) for the establishment of non-replicating persistence (NRP) are poorly understood. In order to investigate mechanisms regulating entry into NRP, we asked how cell cycle regulation is linked to downstream adaptations that ultimately result in NRP. Based on previous reports and our recent studies, we reason that, in order to establish NRP, cells are halted in the cell cycle at the point of septum formation by coupled regulatory mechanisms.    Results  Using bioinformatic consensus modeling, we identified an alternative cell cycle regulatory element, Soj Mtb  encoded by  rv1708 . Soj Mtb  coordinates a regulatory mechanism involving cell cycle control at the point of septum formation and elicits the induction of the MazF6 toxin. MazF6 functions as an mRNA interferase leading to bacteriostasis that can be prevented by interaction with its cognate antitoxin, MazE6. Further, MazEF6 acts independently of other Maz family toxin:antitoxin pairs. Notably,  soj    Mtb    and  mazEF6  transcripts where identified at 20, 40 and 100 days post-infection in increasing abundance indicating a role in adaption during chronic infection.    Conclusions  Here we present the first evidence of a coupled regulatory system in which cell cycle regulation  via  Soj Mtb  is linked to downstream adaptations that are facilitated through the activity of the MazEF6 TA pair.

MazF6 toxin of Mycobacterium tuberculosis demonstrates antitoxin specificity and is coupled to regulation of cell growth by a Soj-like protein