ArticlePLoS pathogens2025
Listeria monocytogenes requires phosphotransferase systems to facilitate intracellular growth and virulence.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Three metabolic pathways replenishing the one-carbon pool collectively support growth and virulence ofeLife · 2026Article
- Sorbose metabolism promotes fitness and virulence inmSphere · 2026Article
- Regulatory Roles of a Novel MarR-like Protein Lmo0840 in Tetracycline-Associated Growth Phenotype and Virulence ofMicroorganisms · 2026Article
- Understanding the role of pyruvate dehydrogenase inInfection and immunity · 2026Article
- High-quality draft genome of the Listeria monocytogenes, one more vaccine strain against livestock listeriosis.Scientific data · 2026Article
- Mechanisms and Therapeutic Potential of Nutritional Immunity.Pathogens (Basel, Switzerland) · 2026Review
- Adaptive microevolution in CC17Frontiers in cellular and infection microbiology · 2026Article
- Adaptive metabolic strategies of intracellular bacterial pathogens.Frontiers in microbiology · 2026Review
- The bacterial phosphotransferase system-mediated rifampicin phosphorylation: ancestral links to rifampicin-inactivating enzyme.Frontiers in microbiology · 2026Article
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Abstract
The metabolism of bacterial pathogens is exquisitely evolved to support virulence in the nutrient-limiting host. Many bacterial pathogens utilize bipartite metabolism to support intracellular growth by splitting carbon utilization between two carbon sources and dividing flux to distinct metabolic needs. For example, previous studies suggest that the professional cytosolic pathogen Listeria monocytogenes (L. monocytogenes) utilizes glycerol and hexose phosphates (e.g., Glucose-6-Phosphate) as catabolic and anabolic carbon sources in the host cytosol, respectively. However, the role of this putative bipartite metabolism in L. monocytogenes virulence has not been fully assessed. Here, we demonstrate that when L. monocytogenes is unable to consume either glycerol (ΔglpD/ΔgolD), hexose phosphates (ΔuhpT), or both (ΔglpD/ΔgolD/ΔuhpT), it is still able to grow in the host cytosol and is 10- to 100-fold attenuated in vivo suggesting that L. monocytogenes consumes alternative carbon source(s) in the host. An in vitro metabolic screen using BioLog's phenotypic microarrays unexpectedly demonstrated that WT and PrfA* (G145S) L. monocytogenes, a strain with constitutive virulence gene expression, use phosphotransferase system (PTS) mediated carbon sources. These findings contrast with the existing metabolic model that cytosolic L. monocytogenes expressing PrfA does not use PTS mediated carbon sources. We next demonstrate that two independent and universal phosphocarrier proteins (PtsI [EI] and PtsH [HPr]), essential for the function of all PTS, are critical for intracellular growth and virulence in vivo. Constitutive virulence gene expression using a PrfA* (G145S) allele in ΔglpD/ΔgolD/ΔuhpT and ΔptsI failed to rescue in vivo virulence defects suggesting phenotypes are due to metabolic disruption and not virulence gene regulation. Finally, in vivo attenuation of ΔptsI and ΔptsH was additive to ΔglpD/ΔgolD/ΔuhpT, suggesting that hexose phosphates and glycerol and PTS mediated carbon source are relevant metabolites. Taken together, these studies indicate that PTS are critical virulence factors for the cytosolic growth and virulence of L. monocytogenes.
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