ArticleNucleic acids research2024
AcrIIIA1 is a protein-RNA anti-CRISPR complex that targets core Cas and accessory nucleases.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- CRISPR-Cas9: Genome Engineering and Future Vaccine Applications.Molecular biotechnology · 2026Review
- Review
- Manipulation of the nucleotide pool in human, bacterial and plant immunity.Nature reviews. Immunology · 2026Review
- Carrot and stick: how RNase R contributes to function and destruction of the translation machinery.RNA biology · 2025Review
- A phage-encoded anti-CRISPR protein co-opts host enolase to prevent type III CRISPR immunity.Nature microbiology · 2025Article
- Structural and molecular mechanisms of an Ro60 homolog from a Thermus bacteriophage.Nucleic acids research · 2025Article
- Mechanism of Cas9 inhibition by AcrIIA11.Nucleic acids research · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
Clustered regularly-interspaced short palindromic repeats (CRISPRs) and CRISPR-associated (Cas) proteins protect bacteria and archaea from their viruses, and anti-CRISPRs (Acrs) are small virus-encoded proteins that inhibit CRISPR-Cas immunity. Over 80 families of Acrs have been described to date; however, only three of these subvert Type III CRISPR-Cas immunity. Type III systems employ a complex network of Cas and accessory nucleases to degrade viral nucleic acids. Here, we discover and characterize AcrIIIA1, the first Type III-A specific anti-CRISPR protein. We demonstrate that AcrIIIA1 binds to Csm2 within the Cas10-Csm effector complex and attenuates Cas10's DNase activity and second messenger production. Additionally, AcrIIIA1 associates with fragmented t(m)RNAs (acrIIIA1-RNAs), and we show that they co-purify with the Cas10-Csm complex during phage infection. Although the precise role(s) of acrIIIA1-RNAs remain unclear, we found that they bind stably to RNase R, a host-encoded nuclease known to bolster immunity, and RNase R has the capacity to degrade them. Altogether, our results support a model in which AcrIIIA1 and its associated RNAs target both core Cas and accessory nucleases to provide robust protection against Type III CRISPR-Cas immunity.
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