RESUMEN
Humans serve as both host and reservoir for Mycobacterium tuberculosis, making tuberculosis a theoretically eradicable disease. How M. tuberculosis alternates between host-imposed quiescence and sporadic bouts of replication to complete its life cycle, however, remains unknown. Here, we identify a metabolic adaptation that is triggered upon entry into hypoxia-induced quiescence but facilitates subsequent cell cycle re-entry. Catabolic remodelling of the cell surface trehalose mycolates of M. tuberculosis specifically generates metabolic intermediates reserved for re-initiation of peptidoglycan biosynthesis. These adaptations reveal a metabolic network with the regulatory capacity to mount an anticipatory response.
Asunto(s)
Ciclo Celular , Pared Celular/metabolismo , Mycobacterium tuberculosis/fisiología , Ácidos Micólicos/metabolismo , Peptidoglicano/metabolismo , Adaptación Fisiológica , Hipoxia , Mycobacterium tuberculosis/metabolismoRESUMEN
Lipidomics is a distinct subspecialty of metabolomics concerned with hydrophobic molecules that organize into membranes. Most of the lipid classes present in Mycobacterium tuberculosis are found only in Actinobacteria and show extreme structural diversity. This article highlights the conceptual basis and the practical challenges associated with the mass spectrometry-based lipidomic study of M. tuberculosis to solve basic questions about the virulence of this lipid-laden organism.