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Updated: May 16, 2026

Overexpressing and Purifying a Toxic Nuclease from Escherichia coli
Published on: August 29, 2025
Host norepinephrine biases codon-dependent virulence translation in EHEC
1Epitranscriptomic and translational responses to antibacterial stress Team, Université Paris Cité, CNRS, Institut de Biologie Physico-Chimique, Expression Génétique Microbienne, Institut Pasteur, Paris, France.
Abstract:
Bacterial pathogens sense host-derived signals to control virulence, yet how these cues shape translation remains unclear. McShane et al. show that the host hormone norepinephrine rewires the tRNA epitranscriptome of enterohemorrhagic Escherichia coli (EHEC) O157:H7, altering wobble-position modifications and shifting decoding capacity toward A/U-ending codons (A. E. C. McShane, C.-K. Chan, R. Chen, M. S. DeMott, et al., mSystems 11:e01418-24, 2026, https://doi.org/10.1128/msystems.01418-25). This bias aligns with the codon architecture of the locus of enterocyte effacement (LEE), a major virulence locus, enabling selective translation of virulence genes. Multi-omic analyses link these changes in tRNA chemistry to proteome remodeling without major shifts in tRNA abundance. By coupling host hormone sensing to codon-biased translation, this work establishes the tRNA epitranscriptome as a dynamic regulator of bacterial virulence.
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