Modulation of bacterial cell size and growth rate via activation of a cell envelope stress response

Bacteria must coordinate their growth rate, shape, and division to survive and flourish, yet how these cellular properties are maintained in the face of environmental stresses is poorly understood. Working with <i>Escherichia coli</i>, we show that activating the Rcs phosphorelay, an envelope stress-signaling system, in the absence of external stresses slows growth, shortens cells, and increases the concentration of the key division protein FtsZ, leading to more closely spaced division sites. Depleting the levels of IgaA, a regulator of the Rcs pathway, yielded similar phenotypes. However, activating Rcs via drug-induced cell-wall disruption did not affect growth rate, indicating that the physiological impact of this pathway depends on the context of activation. Our findings reveal links among cell growth, shape homeostasis, and cell envelope stress. Understanding this coupling further will provide new avenues to predict and modulate bacterial growth and physiology during stress.

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Publication Details

Journal
mBio
Published
2025-09-22
DOI
https://doi.org/10.1128/mbio.02281-25
Citations
2
Primary Topic
Bacterial Genetics and Biotechnology
Type
article
Field-Weighted Citation Impact
3.63
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Modulation of bacterial cell size and growth rate via activation of a cell envelope stress response

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Modulation of bacterial cell size and growth rate via activation of a cell envelope stress response

Jolanda Verheul, Federico Corona, Amanda Miguel, Anna Sueki, David Van Valen, Athanasios Typas, Kerwyn Casey Huang, Matylda Zietek, Handuo Shi, Lisa Maier, Tanneke den Blaauwen
article en
2 citations

Abstract

Bacteria must coordinate their growth rate, shape, and division to survive and flourish, yet how these cellular properties are maintained in the face of environmental stresses is poorly understood. Working with <i>Escherichia coli</i>, we show that activating the Rcs phosphorelay, an envelope stress-signaling system, in the absence of external stresses slows growth, shortens cells, and increases the concentration of the key division protein FtsZ, leading to more closely spaced division sites. Depleting the levels of IgaA, a regulator of the Rcs pathway, yielded similar phenotypes. However, activating Rcs via drug-induced cell-wall disruption did not affect growth rate, indicating that the physiological impact of this pathway depends on the context of activation. Our findings reveal links among cell growth, shape homeostasis, and cell envelope stress. Understanding this coupling further will provide new avenues to predict and modulate bacterial growth and physiology during stress.

mBioVol. 16(11)
California Institute of Technology (US), European Bioinformatics Institute (GB), European Molecular Biology Organization (DE), Heidelberg University (DE), Chan Zuckerberg Initiative (United States) (US), Bioengineering Center (RU), Institute of Natural Science (KP), Amsterdam University of Applied Sciences (NL), Heidelberg University (US), Stanford University (US)
Openalex Percentile: Top 7%
Bacterial Genetics and Biotechnology
3.63
DOIOpen Access PDFOpenAlex
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