ArticleNature communications2025
Trehalose catalytic shift inherently enhances phenotypic heterogeneity and multidrug resistance in Mycobacterium tuberculosis.
Article in Nature communications, 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.
- Stochastic Gene Expression Model with State-Dependent Protein Activation Delay.bioRxiv : the preprint server for biology · 2026Article
- Induced tolerance to UV stress drives survival heterogeneity in isogenic E. coli cell populations.Scientific reports · 2026Article
- Tre-DST: A Drug Susceptibility Test forACS infectious diseases · 2026Article
- Beyond culturability: VBNC-like and differentially culturableFrontiers in cellular and infection microbiology · 2026Review
- Heteroresistance inFrontiers in cellular and infection microbiology · 2026Review
- Prevalence and mechanisms of high-level carbapenem antibiotic tolerance in clinical isolates of Klebsiella pneumoniae.PLoS pathogens · 2026Article
- Drug resistance mechanisms inFrontiers in pharmacology · 2026Review
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16 authors.
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Abstract
Drug-resistance (DR) in bacteria often develops through the repetitive formation of drug-tolerant persisters, which survive antibiotics without genetic changes. It is unclear whether Mycobacterium tuberculosis (Mtb), the bacterium that causes tuberculosis (TB), undergoes a similar transitioning process. Recent studies highlight changes in trehalose metabolism as crucial for persister formation and drug resistance. Here, we observe that mutants lacking trehalose catalytic shift activity exhibited fewer DR mutants due to decreased persisters. This shift enhances Mtb survival during antibiotic treatment by increasing metabolic heterogeneity and drug tolerance, facilitating drug resistance. Rifampicin (RIF)-resistant bacilli display cross-resistance to other antibiotics linked to higher trehalose catalytic shift, explaining how multidrug resistance (MDR) can follow RIF-resistance. In particular, the HN878 W-Beijing strain exhibits higher trehalose catalytic shift, increasing MDR risk. Both genetic and pharmacological inactivation of this shift reduces persister formation and MDR development, suggesting trehalose catalytic shift as a potential therapeutic target to combat TB resistance.
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