ArticleMolecular microbiology2022
Discovery of a novel type IIb RelBE toxin-antitoxin system in Mycobacterium tuberculosis defined by co-regulation with an antisense RNA.
Article in Molecular microbiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 13 citations in OpenAlex.
- From environmental signals to adaptive phenotypes: signal-responsive regulation and network logic of bacterial small RNAs.FEMS microbiology reviews · 2026Review
- Hardwired survival algorithms: RelBE1 and MadR1 couple carbon state to metabolic persistence inFrontiers in microbiology · 2026Article
- Protein-Protein Interactions as Promising Molecular Targets for Novel Antimicrobials Aimed at Gram-Negative Bacteria.International journal of molecular sciences · 2025Review
- The environmental adaptation of acidophilic archaea: promotion of horizontal gene transfer by genomic islands.BMC genomics · 2025Article
- Ser/Thr phosphorylation ofmBio · 2025Article
- Identification of Genes Encoded Toxin-Antitoxin System inInfectious disorders drug targets · 2024Article
- Are all VapC toxins ofJournal of biosciences · 2024Article
- Type II bacterial toxin-antitoxins: hypotheses, facts, and the newfound plethora of the PezAT system.FEMS microbiology reviews · 2023Article
- Impact of Genomic Deletion RD16 on the Expression of theCurrent issues in molecular biology · 2023Article
- Discovery of a novel type IIb RelBE toxin-antitoxin system in Mycobacterium tuberculosis defined by co-regulation with an antisense RNA.Molecular microbiology · 2022Article
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4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Toxin-antitoxin loci regulate adaptive responses to stresses associated with the host environment and drug exposure. Phylogenomic studies have shown that Mycobacterium tuberculosis encodes a naturally expanded type II toxin-antitoxin system, including ParDE/RelBE superfamily members. Type II toxins are presumably regulated exclusively through protein-protein interactions with type II antitoxins. However, experimental observations in M. tuberculosis indicated that additional control mechanisms regulate RelBE2 type II loci under host-associated stress conditions. Herein, we describe for the first time a novel antisense RNA, termed asRelE2, that co-regulates RelE2 production via targeted processing by the Mtb RNase III, Rnc. We find that convergent expression of this coding-antisense hybrid TA locus, relBE2-asrelE2, is controlled in a cAMP-dependent manner by the essential cAMP receptor protein transcription factor, Crp, in response to the host-associated stresses of low pH and nutrient limitation. Ex vivo survival studies with relE2 and asrelE2 knockout strains showed that RelE2 contributes to Mtb survival in activated macrophages and low pH to nutrient limitation. To our knowledge, this is the first report of a novel tripartite type IIb TA loci and antisense post-transcriptional regulation of a type II TA loci.
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