TB is a respiratory illness responsible for the highest mortality rates in the world due to a single bacterium. The unique and complex biology of Mtb bacilli during different stages of TB pathology, and a near-perfect paradigm of a host-pathogen relationship, poses a serious challenge to the development of new therapies for TB eradication. Therefore, an understanding of host-pathogen nexus may help in identifying the key mechanisms for nutritional immunity and metabolic vulnerabilities, which are important to develop new chemotherapeutic strategies. We have previously reported that vitamin B₁₂, which is an indispensable cofactor in all domains of life, is utilised by Mtb for riboswitch-mediated gene expression regulation during planktonic growth and during the reactivation of dormant bacilli. Although non-tuberculous and environmental strains of mycobacteria are generally capable of de novo B₁₂ synthesis, organisms belonging to the MTBC are largely the exception. Yet, the evidence shows that MTBC strains retain the capacity for exogenous uptake – emphasising the relevance of scavenging B₁₂ for the physiology of MTBC. My current research aims to elucidate the mechanisms of vitamin B₁₂ uptake and its utilization for Mtb physiology and virulence using a combination of molecular approaches, including proximity labeling and protein mass spectrometry, ribosome profiling, microscopy, and in vivo models.