ArticleApplied and environmental microbiology2015
Mutational Analysis of the Antitoxin in the Lactococcal Type III Toxin-Antitoxin System AbiQ.
Article in Applied and environmental microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Deciphering the RNA-based regulation mechanism of the phage-encoded AbiF system in Clostridioides difficile.PLoS genetics · 2025Article
- Bioinformatic exploration reveals features of tenpIN family of type III toxin-antitoxin systems in bacteria and viruses.Scientific reports · 2025Article
- Toxin-antitoxin systems and their medical applications: current status and future perspective.Applied microbiology and biotechnology · 2021Review
- Substrate specificity of bacterial endoribonuclease toxins.BMB reports · 2020Review
- Article
- The bacterial Type III toxin-antitoxin system, ToxIN, is a dynamic protein-RNA complex with stability-dependent antiviral abortive infection activity.Scientific reports · 2018Article
- Environmental T4-Family Bacteriophages Evolve to Escape Abortive Infection via Multiple Routes in a Bacterial Host Employing "Altruistic Suicide" through Type III Toxin-Antitoxin Systems.Frontiers in microbiology · 2017Article
- Review
- Toxin-Antitoxin Systems of Staphylococcus aureus.Toxins · 2016Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lactococcal abortive phage infection mechanism AbiQ recently was classified as a type III toxin-antitoxin system in which the toxic protein (ABIQ) is regulated following cleavage of its repeated noncoding RNA antitoxin (antiQ). In this study, we investigated the role of the antitoxin in antiphage activity. The cleavage of antiQ by ABIQ was characterized using 5' rapid amplification of cDNA ends PCR and was located in an adenine-rich region of antiQ. We next generated a series of derivatives with point mutations within antiQ or with various numbers of antiQ repetitions. These modifications were analyzed for their effect on the antiphage activity (efficiency of plaquing) and on the endoribonuclease activity (Northern hybridization). We observed that increasing or reducing the number of antiQ repeats significantly decreased the antiphage activity of the system. Several point mutations had a similar effect on the antiphage activity and were associated with changes in the digestion profile of antiQ. Interestingly, a point mutation in the putative pseudoknot structure of antiQ mutants led to an increased AbiQ antiphage activity, thereby offering a novel way to increase the activity of an abortive infection mechanism.
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