Metabolism of the gram-positive bacterial pathogen listeria monocytogenes

The bacterial pathogen Listeria monocytogenes is well adapted to life in the soil and on vegetation as a saprophyte (i.e., extracellular environments) and to life in the cytosol of mammalian cells as a pathogen (i.e., intracellular environment). These environments differ greatly in their metabolite repertoires (e.g., carbon, sulfur, and nitrogen sources) and abundance (e.g., amino acid availability). Therefore, L. monocytogenes requires niche-specific adaptations to support growth and uses metabolic cues to trigger virulence mechanisms, such as the master virulence regulator, PrfA (1). The complete metabolic potential of L. monocytogenes has been inferred bioinformatically from genomic (2-5) and transcriptomic studies (1, 6-8), as well as experimentally using both defined media as a test for auxotrophy (9-12) and more recently by isotopologue metabolomics (13, 14). While these studies have certainly taught us much about L. monocytogenes’ metabolic potential, it is important to note that, given the wide array of environments L. monocytogenes is capable of inhabiting, our understanding of its metabolic potential and how strain to strain variation might affect this potential, is incomplete.