ArticleNature communications2023
MenT nucleotidyltransferase toxins extend tRNA acceptor stems and can be inhibited by asymmetrical antitoxin binding.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Ribosomal RNA cleavage by the previously unidentified RelS-RelI toxin-antitoxin system controls growth of Mycobacterium tuberculosis.Nucleic acids research · 2026Article
- Identification of potential MenT3 inhibitors for Mycobacterium tuberculosis using the generative artificial intelligence and SilicoXplore platform.Scientific reports · 2026Article
- A single viral enzyme drives tRNA-dependent hypermodification of DNA at adenine.Nature communications · 2026Article
- Carrot and stick: how RNase R contributes to function and destruction of the translation machinery.RNA biology · 2025Review
- Ribonuclease toxin RelE1 inhibits growth of Mycobacterium tuberculosis through specific cleavage of the ribosomal anti-Shine-Dalgarno region.Nucleic acids research · 2025Article
- Nucleotidyltransferase toxin MenT extends aminoacyl acceptor ends of serine tRNAs to control Mycobacterium tuberculosis growth.Nature communications · 2024Article
- Inducible auto-phosphorylation regulates a widespread family of nucleotidyltransferase toxins.Nature communications · 2024Article
- Mycobacterium tuberculosis strain with deletions in menT3 and menT4 is attenuated and confers protection in mice and guinea pigs.Nature communications · 2024Article
- Substrate specificity of Mycobacterium tuberculosis tRNA terminal nucleotidyltransferase toxin MenT3.Nucleic acids research · 2024Article
- Article
- Recognition of the tRNA structure: Everything everywhere but not all at once.Cell chemical biology · 2024Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis, the bacterium responsible for human tuberculosis, has a genome encoding a remarkably high number of toxin-antitoxin systems of largely unknown function. We have recently shown that the M. tuberculosis genome encodes four of a widespread, MenAT family of nucleotidyltransferase toxin-antitoxin systems. In this study we characterize MenAT1, using tRNA sequencing to demonstrate MenT1 tRNA modification activity. MenT1 activity is blocked by MenA1, a short protein antitoxin unrelated to the MenA3 kinase. X-ray crystallographic analysis shows blockage of the conserved MenT fold by asymmetric binding of MenA1 across two MenT1 protomers, forming a heterotrimeric toxin-antitoxin complex. Finally, we also demonstrate tRNA modification by toxin MenT4, indicating conserved activity across the MenT family. Our study highlights variation in tRNA target preferences by MenT toxins, selective use of nucleotide substrates, and diverse modes of MenA antitoxin activity.
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