ArticlePLoS pathogens2016
The Listeria monocytogenes PASTA Kinase PrkA and Its Substrate YvcK Are Required for Cell Wall Homeostasis, Metabolism, and Virulence.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed.
- Post-translational modifications of GlmR integrate metabolic and stress signals to maintain cell envelope homeostasis in Bacillus subtilis.PLoS genetics · 2026Article
- Stk1 is required for BlaR1-mediated broad-spectrum β-lactam resistance in epidemic-causing strains ofResearch square · 2026Article
- Staying in the loop to make ends meet: roles and regulation of GlmR inbioRxiv : the preprint server for biology · 2025Article
- Structural and evolutionary insights into understudied bacterial serine-threonine pseudokinase families.Biochemical Society transactions · 2025Review
- Listeria monocytogenes: from a saprophytic to a cytosolic virulent pathogen.World journal of microbiology & biotechnology · 2025Review
- An atlas of bacterial serine-threonine kinases reveals functional diversity and key distinctions from eukaryotic kinases.Science signaling · 2025Article
- Population structure and gene flux ofMicrobial genomics · 2025Article
- Reciprocal regulation of enterococcal cephalosporin resistance by products of the autoregulated yvcJ-glmR-yvcL operon enhances fitness during cephalosporin exposure.PLoS genetics · 2024Article
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- On the mechanisms of lysis triggered by perturbations of bacterial cell wall biosynthesis.Nature communications · 2023Article
- A link between STK signalling and capsular polysaccharide synthesis in Streptococcus suis.Nature communications · 2023Article
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- Mutations inmBio · 2023Article
- Phosphorylation of GntR reduces Streptococcus suis oxidative stress resistance and virulence by inhibiting NADH oxidase transcription.PLoS pathogens · 2023Article
- Article
- Identification of serine/threonine kinases that regulate metabolism and sporulation in Clostridium beijerinckii.Applied microbiology and biotechnology · 2022Article
- Arginine glycosylation regulates UDP-GlcNAc biosynthesis in Salmonella enterica.Scientific reports · 2022Article
- MurA escape mutations uncouple peptidoglycan biosynthesis from PrkA signaling.PLoS pathogens · 2022Article
- IreK-Mediated, Cell Wall-Protective Phosphorylation inJournal of proteome research · 2021Article
- Article
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11 authors.
Funding
Abstract
Obstacles to bacterial survival and replication in the cytosol of host cells, and the mechanisms used by bacterial pathogens to adapt to this niche are not well understood. Listeria monocytogenes is a well-studied Gram-positive foodborne pathogen that has evolved to invade and replicate within the host cell cytosol; yet the mechanisms by which it senses and responds to stress to survive in the cytosol are largely unknown. To assess the role of the L. monocytogenes penicillin-binding-protein and serine/threonine associated (PASTA) kinase PrkA in stress responses, cytosolic survival and virulence, we constructed a ΔprkA deletion mutant. PrkA was required for resistance to cell wall stress, growth on cytosolic carbon sources, intracellular replication, cytosolic survival, inflammasome avoidance and ultimately virulence in a murine model of Listeriosis. In Bacillus subtilis and Mycobacterium tuberculosis, homologues of PrkA phosphorylate a highly conserved protein of unknown function, YvcK. We found that, similar to PrkA, YvcK is also required for cell wall stress responses, metabolism of glycerol, cytosolic survival, inflammasome avoidance and virulence. We further demonstrate that similar to other organisms, YvcK is directly phosphorylated by PrkA, although the specific site(s) of phosphorylation are not highly conserved. Finally, analysis of phosphoablative and phosphomimetic mutants of YvcK in vitro and in vivo demonstrate that while phosphorylation of YvcK is irrelevant to metabolism and cell wall stress responses, surprisingly, a phosphomimetic, nonreversible negative charge of YvcK is detrimental to cytosolic survival and virulence in vivo. Taken together our data identify two novel virulence factors essential for cytosolic survival and virulence of L. monocytogenes. Furthermore, our data demonstrate that regulation of YvcK phosphorylation is tightly controlled and is critical for virulence. Finally, our data suggest that yet to be identified substrates of PrkA are essential for cytosolic survival and virulence of L. monocytogenes and illustrate the importance of studying protein phosphorylation in the context of infection.
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