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<p>The Rcs signal transduction system is a phosphorelay responsible for sensing enterobacterial cell envelope stresses. In <i>Escherichia coli</i>, 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 <i>E. coli</i> 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.</p>

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Bacterial cell widening alters periplasmic size and activates envelope stress responses

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月3日

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  • Matylda Zietek,
  • Amanda Miguel,
  • Handuo Shi,
  • Iskander Khusainov,
  • Abir T Asmar,
  • Sri Ram,
  • Morgane Wartel,
  • Anna Sueki,
  • Martin Schorb,
  • Mark Goulian,
  • Jean-François Collet,
  • Martin Beck,
  • Kerwyn Casey Huang,
  • Athanasios Typas

摘要

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.