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Bacterial cell wall biosynthesis is controlled by growth rate dependent modulation of turgor pressure in E. coli
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Bacterial cell wall biosynthesis is controlled by growth rate dependent modulation of turgor pressure in E. coli

Avik Mukherjee, Yanqing Huang, Seungeun Oh +10 more
May 2025
 ·
bioRxiv
 ·
DOI 
10.1101/2023.08.31.555748
94
%
Reproducible
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It ranks in the top 1% of preprints assessed in Microbiology this quarter.
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Why this is interesting

This work overturns the assumption that E. coli cell wall growth is turgor-independent, revealing instead that rRNA counterions tune turgor pressure with growth rate, making turgor the pacemaker for envelope expansion and density homeostasis.

QED claims analysis

Summary

Turgor pressure in E. coli increases with growth rate through ribosomal RNA-mediated accumulation of potassium counterions, and this growth rate-dependent turgor pressure directly controls cell wall biosynthesis rate, thereby simultaneously achieving biomass density homeostasis and coordinating cell wall expansion with cytoplasmic biomass production without requiring fine-tuned regulatory mechanisms.

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Main Claim 1 –

E. coli turgor pressure increases with growth rate

Supporting evidence

  • Higher growth-rate turgor is driven by increased intracellular potassium
  • Ribosomal RNA negative charge drives potassium-mediated turgor increases
  • Mechano-electro-osmotic model predicts ribosome-dependent turgor scaling
Main Claim 2 –

Turgor pressure directly controls E. coli cell wall biosynthesis rate

Supporting evidence

  • Endopeptidase abundance alters cell wall viscosity and turgor expansion
  • Reduced crosslinking lowers elastic modulus, modulating turgor-driven expansion
Main Claim 3 –

E. coli biomass density remains constant across growth rates

Supporting evidence

  • Cytoplasmic charge balance regulates biomass density via turgor pressure
  • Cell width modulates biomass density via turgor-generated wall tension

Abstract

The cell wall is an essential cellular component of bacteria and the target of many antibiotics. However, how bacteria regulate the rate of cell wall biosynthesis as growth rates change remains unresolved. In E. coli, cell wall growth was thought to proceed independently from turgor pressure, the osmotic pressure that the cytoplasm exerts on the cell wall. Here, we uncover a striking increase of turgor pressure with growth rate. Modulating turgor pressure and measuring cell wall biosynthesis, we find that turgor pressure is directly controls the rate of cell wall biosynthesis. The picture that emerges is that turgor pressure is largely generated by counterions of negatively charged cellular biomass. The increase in turgor pressure with growth rates results from more ribosomes and therefore higher concentrations of negatively charged ribosomal RNA. Elegantly, the coupling between biomass composition, turgor pressure and cell wall biosynthesis simultaneously explains how bacteria achieve homeostasis of cytoplasmic crowding and how they regulate the rate of cell wall biosynthesis across growth rates.

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