ArticleCell reports2025
A mutation in RNA polymerase imparts resistance to β-lactams by preventing dysregulation of amino acid and nucleotide metabolism.
Article in Cell reports, 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.
- Mutations in RNA polymerase that drive the emergence of antibiotic resistance.Current opinion in microbiology · 2026Review
- Post-translational modifications of GlmR integrate metabolic and stress signals to maintain cell envelope homeostasis in Bacillus subtilis.PLoS genetics · 2026Article
- Global response to antibiotic exposure reveals a critical role for nucleotide metabolism in high-level β-lactam tolerance.npj antimicrobials and resistance · 2026Article
- ThebioRxiv : the preprint server for biology · 2025Article
- Staying in the loop to make ends meet: roles and regulation of GlmR inbioRxiv : the preprint server for biology · 2025Article
- Global response to antibiotic exposure uncovers a critical role for nucleotide metabolism in high-level β-lactam tolerance.Research square · 2025Article
- Metabolic rewiring of isoniazid sensitivity inProceedings of the National Academy of Sciences of the United States of America · 2025Article
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2 authors.
Funding
Abstract
Resistance to diverse antibiotics can result from mutations in RNA polymerase (RNAP), but the underlying mechanisms remain poorly understood. In this study, we compare two Bacillus subtilis RNAP mutations: one in β' (rpoC G1122D) that increases resistance to cefuroxime (CEF; a model β-lactam) and one in β (rpoB H482Y) that increases sensitivity. CEF resistance is mediated by a decrease in branched-chain amino acid (BCAA), methionine, and pyrimidine pathways. These same pathways are upregulated by CEF, and their derepression increases CEF sensitivity and antibiotic-induced production of reactive oxygen species. The CEF-resistant rpoC G1122D mutant evades these metabolic perturbations, and repression of the BCAA and pyrimidine pathways may function to restrict membrane biogenesis, which is beneficial when cell wall synthesis is impaired. These findings provide a vivid example of how RNAP mutations, which commonly arise in response to diverse selection conditions, can rewire cellular metabolism to enhance fitness.
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