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Almost 140 years after the identification of  Mycobacterium tuberculosis  as the etiological agent of tuberculosis, important aspects of its biology remain poorly described. Little is known about the role of posttranscriptional control of gene expression and RNA biology, including the role of most of the small RNAs (sRNAs) identified to date. We have carried out a detailed investigation of the  M. tuberculosis  sRNA F6 and shown it to be dependent on SigF for expression and significantly induced in starvation conditions  in vitro  and in a mouse model of infection. Further exploration of F6 using an  in vitro  starvation model of infection indicates that F6 affects the expression of the essential chaperonins GroEL2 and GroES. Our results point toward a role for F6 during periods of low metabolic activity typically associated with long-term survival of  M. tuberculosis  in human granulomas.   IMPORTANCE  Control of gene expression via small regulatory RNAs (sRNAs) is poorly understood in one of the most successful pathogens,  Mycobacterium tuberculosis . Here, we present an in-depth characterization of the sRNA F6, including its expression in different infection models and the differential gene expression observed upon deletion of the sRNA. Our results demonstrate that deletion of F6 leads to dysregulation of the two essential chaperonins GroEL2 and GroES and, moreover, indicate a role for F6 in the long-term survival and persistence of  M. tuberculosis  in the human host.

The Mycobacterium tuberculosis sRNA F6 Modifies Expression of Essential Chaperonins, GroEL2 and GroES