Comprehensive Functional Analysis of Mycobacterium tuberculosis Toxin-Antitoxin Systems: Implications for Pathogenesis, Stress Responses, and Evolution
Figure 7
Model of stress-induced TA system activation and proteome remodeling.
(A) Under normal growth conditions, the antitoxin is bound to its cognate toxin, this complex in turn binds its own promoter, inhibiting transcription. (B) In response to stress, the antitoxin is specifically degraded, releasing the toxin to cleaves existing transcripts. Additionally, degradation of the antitoxin results in increased transcription of the TA system. (C) Upon stabilization of the antitoxin, the TA system is inactivated and toxin-antitoxin complex, resulting in transcriptional inhibition of its operon. This pulse of toxin activity functionally erases the previous transcriptional profile allowing the newly stress induced messages to be preferentially translated.