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.
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.
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.
Mycobacterium tuberculosis (Mtb), effectors secreted through SecA2 pathway cause double strand breaks (DSBs) in the host DNA, which in turn activates ATM kinase to gain survival advantages, through Akt.
Time-lapse live cell imaging of single Mycobacterium tuberculosis bacilli growing into small colonies enables their rapid phenotypic characterization including anti-microbial resistance and heteroresistance in clinical isolates.