Cofactor F420 is essential in the metabolism of archaea and a wide range of bacteria, acting as a hydride transfer agent. We investigate the role of the F420 biosynthetic and metabolic pathways in microbial biochemistry and physiology. This line of research has implications in understanding pathogenesis of M. tuberculosis and agricultural methane emissions.
Central Metabolism in M. tuberculosis
Tuberculosis (TB) is the leading cause of death globally from a single infectious agent, accounting for around 1.5 million deaths each year. The success of the M. tuberculosis as a pathogen lies in its ability to survive in a dormant state within host cells for several decades, awaiting the right moment to “wake up”. We investigate essential metabolic features that enable M. tuberculosis to persist under such conditions, with the ultimate goal of developing inhibitors as potential antitubercular agents.
Iron metabolism is essential for the survival and pathogenicity of M. tuberculosis. We are interested in how iron-dependent proteins acquire iron and use it to support mycobacterial metabolism. Our focus is on the biogenesis and regulation of iron-sulfur clusters, which can detect environmental cues and modulate bacterial metabolism in response to harsh conditions encountered inside host cells. This research will enable us to identify novel therapeutic targets for the treatment of tuberculosis.
Microbial Secondary Metabolites
Microbial secondary metabolites provide a rich and diverse source of bioactive molecules. We seek to discover and exploit secondary metabolites possessing antimicrobial properties. Our multidisciplinary research combines metagenomics, chemical synthesis, and biosynthetic pathways to develop innovative strategies for combating antimicrobial resistance.