ArticleThe EMBO journal2025
Bacterial cell widening alters periplasmic size and activates envelope stress responses.
Article in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Bacterial growth under confinement requires transcriptional adaptation to resist turgor pressure build-up.Nature communications · 2026Article
- Bacterial extracellular vesicles promote membrane repair and tolerance to polymyxin B.Science advances · 2026Article
- Different Cell Wall Compositions of ESKAPE Isolates on Glass Surfaces Impact Adhesion Adaptability to Dynamic Shear Stress.Microorganisms · 2026Article
- Modulation of bacterial cell size and growth rate via activation of a cell envelope stress response.mBio · 2025Article
- Bactericidal effect of tetracycline in E. coli strain ED1a may be associated with ribosome dysfunction.Nature communications · 2024Article
- Article
- Physiological and regulatory convergence between osmotic and nutrient stress responses in microbes.Current opinion in cell biology · 2023Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
The Rcs signal transduction system is a phosphorelay responsible for sensing enterobacterial cell envelope stresses. In Escherichia coli, the Rcs system is required to survive treatment with A22 and mecillinam, antibiotics that perturb cell size. To test whether size changes are correlated with envelope damage and thereby sensed by the Rcs system, we tuned E. coli cell size via A22 treatment, mutations in the cell-shape determinant MreB, and mechanically confined growth. In all conditions, cell width was strongly correlated with Rcs activation, and RcsF, the outer-membrane-localized upstream component, was essential for responding to cell width changes. Several gene deletions that induce Rcs resulted in cells that were wider than wild-type. Cryo-electron microscopy revealed that the periplasm of a wide MreB mutant is ~3 nm thinner than in wild-type cells, bringing RcsF closer to the downstream, inner-membrane-localized components of the signaling cascade. Conversely, extending the RcsF linker region in wild-type cells by ~3 nm increased Rcs activity. Thus, we propose that the Rcs system responds to changes in cell width due to altered periplasmic thickness.
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Registered trials
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