ArticlePLoS pathogens2022
Loss of RNase J leads to multi-drug tolerance and accumulation of highly structured mRNA fragments in Mycobacterium tuberculosis.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 42 citations in OpenAlex.
- The structural context of mutations in proteins predicts their effect on antibiotic resistance.eLife · 2026Article
- Population-level genome sequencing reveals distinctmSystems · 2026Article
- Comparative genomics and transcriptomics of rough and smooth Mycobacterium marinum focusing on ESX-1, ESX-6 and LOS genes.Scientific reports · 2026Article
- Heterogeneity in microbial antibiotic responses: genetic basis and within-host evolution.Trends in genetics : TIG · 2026Review
- PE/PPE proteins contribute to Mycobacterium tuberculosis drug resistance.Nature communications · 2026Article
- Population-level genome sequencing reveals distinct Mycobacterium tuberculosis intrahost mutational trajectories in simian immunodeficiency virus co-infected and antiretroviral treated non-human primates.bioRxiv : the preprint server for biology · 2026Article
- New Chemical Scaffold with Antimicrobial Activity Identified in a Screening of Industrial Photoactive Compounds.Antibiotics (Basel, Switzerland) · 2026Article
- Mycobacterium tuberculosis MutT4/RppH is an RNA pyrophosphohydrolase that forms condensate-like bodies and impacts mRNA degradation.Nucleic acids research · 2026Article
- Drug resistance mechanisms inFrontiers in pharmacology · 2026Review
- Alternative nucleic acid structures in microbial biology: regulatory functions and antimicrobial opportunities.Frontiers in cellular and infection microbiology · 2026Review
- Protein Architecture and Composition in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Defining the role of RNase E in the mycobacterial degradosome-like network.bioRxiv : the preprint server for biology · 2025Article
- Article
- Antibiotic tolerance & resilience in M. tuberculosis: Potential to predict & pre-empt antibiotic resistance.The Indian journal of medical research · 2025Article
- The structural context of mutations in proteins predicts their effect on antibiotic resistance.bioRxiv : the preprint server for biology · 2025Article
- Genetic determinants ofMicrobiology spectrum · 2025Article
- PPE50 variants as novel phylogeographic signatures of host-pathogen co-evolution in tuberculosis.Communications biology · 2025Article
- Integrating genomic, transcriptomic, and phenotypic information to explore drug resistance in Mycobacterium tuberculosis sub-lineage 4.2.2.2.Journal of applied microbiology · 2025Article
- Analysis of complete genomes of Mycobacterium tuberculosis sublineage 2.1 (Proto-Beijing) revealed the presence of three pe_pgrs3-pe_pgrs4-like genes.Scientific reports · 2024Article
- Functional Analysis of Promoters, mRNA Cleavage, and mRNA Secondary Structure onPathogens (Basel, Switzerland) · 2024Article
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8 authors at 2 institutions in 1 country.
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Abstract
Despite the existence of well-characterized, canonical mutations that confer high-level drug resistance to Mycobacterium tuberculosis (Mtb), there is evidence that drug resistance mechanisms are more complex than simple acquisition of such mutations. Recent studies have shown that Mtb can acquire non-canonical resistance-associated mutations that confer survival advantages in the presence of certain drugs, likely acting as stepping-stones for acquisition of high-level resistance. Rv2752c/rnj, encoding RNase J, is disproportionately mutated in drug-resistant clinical Mtb isolates. Here we show that deletion of rnj confers increased tolerance to lethal concentrations of several drugs. RNAseq revealed that RNase J affects expression of a subset of genes enriched for PE/PPE genes and stable RNAs and is key for proper 23S rRNA maturation. Gene expression differences implicated two sRNAs and ppe50-ppe51 as important contributors to the drug tolerance phenotype. In addition, we found that in the absence of RNase J, many short RNA fragments accumulate because they are degraded at slower rates. We show that the accumulated transcript fragments are targets of RNase J and are characterized by strong secondary structure and high G+C content, indicating that RNase J has a rate-limiting role in degradation of highly structured RNAs. Taken together, our results demonstrate that RNase J indirectly affects drug tolerance, as well as reveal the endogenous roles of RNase J in mycobacterial RNA metabolism.
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