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Background  The ability of  Mycobacterium tuberculosis  to establish a latent infection (LTBI) in humans confounds the treatment of tuberculosis. Consequently, there is a need to discover new therapeutic agents that can kill  M. tuberculosis  both during active disease and LTBI. The streptomycin-dependent strain of  M. tuberculosis , 18b, provides a useful tool for this purpose since upon removal of streptomycin (STR) it enters a non-replicating state that mimics latency both  in vitro  and in animal models.    Results  The 4.41 Mb genome sequence of  M. tuberculosis  18b was determined and this revealed the strain to belong to clade 3 of the ancient ancestral lineage of the Beijing family. STR-dependence was attributable to insertion of a single cytosine in the 530 loop of the 16S rRNA and to a single amino acid insertion in the N-terminal domain of initiation factor 3. RNA-seq was used to understand the genetic programme activated upon STR-withdrawal and hence to gain insight into LTBI. This revealed reconfiguration of gene expression and metabolic pathways showing strong similarities between non-replicating 18b and  M. tuberculosis  residing within macrophages, and with the core stationary phase and microaerophilic responses.    Conclusion  The findings of this investigation confirm the validity of 18b as a model for LTBI, and provide insight into both the evolution of tubercle bacilli and the functioning of the ribosome.    Electronic supplementary material  The online version of this article (doi:10.1186/s12864-016-2528-2) contains supplementary material, which is available to authorized users.

Genomic and transcriptomic analysis of the streptomycin-dependent Mycobacterium tuberculosis strain 18b