M. tuberculosis, the bacterium that causes the disease tuberculosis, uses a signaling system that senses multiple products of the host's immune system to modify gene expression to colonize the lung.

Metabolomics and stable isotope labelling studies of virulent Mycobacterium tuberculosis reveal a de-centralised metabolic network able to utilise various amino acids as nitrogen sources to a better extent than ammonium.

Cryo-electron microscopy structures show how the clinically used antimicrobial fidaxomicin binds and inhibits Mycobacterium tuberculosis RNA polymerase by acting like a doorstop to jam the enzyme in an open conformation via the general transcription factor RbpA.

The ubiquitous second messenger cyclic AMP, produced by Rv3645/MacE, controls long-chain fatty acid metabolism and intrinsic multidrug resistance in M. tuberculosis.

A study of tuberculosis cases in the Karonga district of Malawi reveals that the main lineages of M. tuberculosis differ in their transmission patterns and virulence.

A crowd of inexperienced volunteers can reproducibily and accurately measured how effective a panel of antibiotics are in treating a M. tuberculosis sample.

Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.

Mycobacterium tuberculosis penetrates the airway mucosa through M cells via the mycobacterial virulence factor EsxA and the host M cell surface receptor scavenger receptor B1.

The anti-tuberculosis drug bedaquiline reprograms human macrophages into potent bactericidal phagocytes, which are able to control bacterial infection.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.