ArticlePLoS genetics2025
Coordination of cell envelope biology by Escherichia coli MarA protein potentiates intrinsic antibiotic resistance.
Article in PLoS genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biofilm-mediated antibiotic tolerance in bacterial pathogens: Integrated molecular networks and novel therapeutic avenues.Virulence · 2026Review
- Thermal Shifts Dominate Single-Gene Responses to Transcription-Targeting Antibiotics.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of bacterial transcription by distortion of promoter base pairing.Nucleic acids research · 2026Article
- MarA binds and activates the ABC efflux pump YadGH to confer conditional macrolide resistance in AcrB-deficientFrontiers in microbiology · 2026Article
- EnteroaggregativeFrontiers in microbiology · 2025Article
- Integration host factor regulates antibiotic susceptibility through modulating alanine metabolism inFrontiers in microbiology · 2025Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The multiple antibiotic resistance activator (MarA) protein is a transcription factor implicated in control of intrinsic antibiotic resistance in enteric bacterial pathogens. In this work, we screened the Escherichia coli genome computationally for MarA binding sites. By incorporating global maps of transcription initiation, and clustering predicted targets according to gene function, we were able to avoid widespread misidentification of MarA sites, which has hindered prior studies. Subsequent genetic and biochemical analyses identified direct activation of genes for lipopolysaccharide (LPS) biosynthesis and repression of a cell wall remodelling endopeptidase. Rewiring of the MarA regulon, by mutating subsets of MarA binding sites, reveals synergistic interactions between regulatory targets of MarA. Specifically, we show that uncoupling LPS production, or cell wall remodelling, from regulation by MarA, renders cells hypersensitive to mutations altering lipid trafficking by the MlaFEDCB system. Together, our findings demonstrate how MarA co-regulates different aspects of cell envelope biology to maximise antibiotic resistance.
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Registered trials
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