ArticleMolecular microbiology2023
PASTA-kinase-mediated signaling drives accumulation of the peptidoglycan synthesis protein MurAA to promote cephalosporin resistance in Enterococcus faecalis.
Article in Molecular microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Artificial Sweeteners Induce Bacterial Drug Resistance and Modulate Gene Expression.Infection and drug resistance · 2026Article
- Phosphorylation of the cell wall hydrolase MltG in response to cell wall stress modulates resistance toward cephalosporins inJournal of bacteriology · 2025Article
- The cell wall hydrolase MltG is essential to maintain cell wall homeostasis ofJournal of bacteriology · 2025Article
- Article
- TheFrontiers in microbiology · 2025Article
- GpsB Coordinates StkP Signaling as a PASTA Kinase Adaptor in Streptococcus pneumoniae Cell Division.Journal of molecular biology · 2024Article
- Pbp4 provides transpeptidase activity to the FtsW-PbpB peptidoglycan synthase to drive cephalosporin resistance inAntimicrobial agents and chemotherapy · 2024Article
- Reciprocal regulation of enterococcal cephalosporin resistance by products of the autoregulated yvcJ-glmR-yvcL operon enhances fitness during cephalosporin exposure.PLoS genetics · 2024Article
- Secrets of getting started: Regulation of the first committed step of peptidoglycan synthesis by protein phosphorylation in Enterococcus and other Gram-positive bacteria.Molecular microbiology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The bacterial PASTA kinase, IreK, is required for intrinsic cephalosporin resistance in the Gram-positive opportunistic pathogen, Enterococcus faecalis. IreK activity is enhanced in response to cell wall stress, such as cephalosporin exposure. The downstream consequences of IreK activation are not well understood in E. faecalis, but recent work in other low-GC Gram-positive bacteria demonstrated PASTA kinase-dependent regulation of MurAA, an enzyme that performs the first committed step in the peptidoglycan synthesis pathway. Here, we used genetic suppressor selections to identify MurAA as a downstream target of IreK signaling in E. faecalis. Using complementary genetic and biochemical approaches, we demonstrated that MurAA abundance is regulated by IreK signaling in response to physiologically relevant cell wall stress to modulate substrate flux through the peptidoglycan synthesis pathway. Specifically, the IreK substrate, IreB, promotes proteolysis of MurAA through a direct physical interaction in a manner responsive to phosphorylation by IreK. MurAB, a homolog of MurAA, also promotes MurAA proteolysis and interacts directly with IreB. Our results therefore establish a connection between the cell wall stress sensor IreK and one critical physiological output to modulate peptidoglycan synthesis and drive cephalosporin resistance.
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