ArticleMolecular cell2022
Mycobacterium abscessus HelR interacts with RNA polymerase to confer intrinsic rifamycin resistance.
Article in Molecular cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- The SigD regulon of Mycobacterium abscessus determines cell envelope composition and antibiotic susceptibility.PLoS genetics · 2026Article
- Review
- Bacteria sense the antibiotic rifampicin through a widespread dual-promoter based alarm system.Nucleic acids research · 2026Article
- The bacterial phosphotransferase system-mediated rifampicin phosphorylation: ancestral links to rifampicin-inactivating enzyme.Frontiers in microbiology · 2026Article
- Emerging antibiotic resistance by various novel proteins/enzymes.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Review
- RapA opens the RNA polymerase clamp to disrupt post-termination complexes and prevent cytotoxic R-loop formation.Nature structural & molecular biology · 2025Article
- Curcumin-mediated antimicrobial photodynamic therapy for inactivating Mycobacterium abscessus: a promising approach for non-tuberculous mycobacterial skin infections.Lasers in medical science · 2025Article
- Mycobacterial HelD connects RNA polymerase recycling with transcription initiation.Nature communications · 2024Article
- Distinct Effects of Moxifloxacin and Bedaquiline on Growing and 'Non-Culturable'Microorganisms · 2023Article
- What the Hel: recent advances in understanding rifampicin resistance in bacteria.FEMS microbiology reviews · 2023Article
- CRISPR Interference-Based Inhibition of MAB_0055c Expression Alters Drug Sensitivity in Mycobacterium abscessus.Microbiology spectrum · 2023Article
- Multiple classes and isoforms of the RNA polymerase recycling motor protein HelD.MicrobiologyOpen · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Rifampicin (RIF), the frontline drug against M. tuberculosis, is completely ineffective against M. abscessus, partially due to the presence of an ADP-ribosyltransferase (Arr) that inactivates RIF. Using RNA-seq, we show that exposure of M. abscessus to sublethal doses of RIF and Rifabutin (RBT), a close analog of RIF, results in an ∼25-fold upregulation of Mab_helR in laboratory and clinical isolates. An isogenic deletion in Mab_helR results in RIF/RBT hypersensitivity, and overexpression of Mab_helR confers RIF tolerance in M. tuberculosis. We demonstrate an increased HelR-RNAP association in RIF-exposed bacteria and a MabHelR-mediated dissociation of RNAP from stalled initiation complexes in vitro. Finally, we show that the tip of the PCh-loop of Mab_helR, present in proximity to RIF, is critical for conferring RIF resistance but dispensable for dissociation of stalled RNAP complexes, suggesting that HelR-mediated RIF resistance requires a step in addition to displacement of RIF-stalled RNAP.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.