ArticleNature communications2020
Structural basis for inhibition of an archaeal CRISPR-Cas type I-D large subunit by an anti-CRISPR protein.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- An anti-CRISPR targets the sgRNA to block Cas9 and guides the design of enhanced genome editors.Nature structural & molecular biology · 2026Article
- Research Progress on the Mechanism and Application of the Type I CRISPR-Cas System.International journal of molecular sciences · 2024Review
- Taxonomic Distribution, Phylogenetic Relationship, and Domain Conservation of CRISPR-Associated Cas Proteins.Bioinformatics and biology insights · 2024Article
- The biology and type I/III hybrid nature of type I-D CRISPR-Cas systems.The Biochemical journal · 2023Review
- Functional and Phylogenetic Diversity of Cas10 Proteins.The CRISPR journal · 2023Article
- Type I CRISPR-Cas-mediated microbial gene editing and regulation.AIMS microbiology · 2023Review
- Structure and mechanism of the type I-G CRISPR effector.Nucleic acids research · 2022Article
- Structural rearrangements allow nucleic acid discrimination by type I-D Cascade.Nature communications · 2022Article
- Insights into the inhibition of type I-F CRISPR-Cas system by a multifunctional anti-CRISPR protein AcrIF24.Nature communications · 2022Article
- Expanding the plant genome editing toolbox with recently developed CRISPR-Cas systems.Plant physiology · 2022Review
- Metal Dependence and Functional Diversity of Type I Cas3 Nucleases.Biochemistry · 2022Article
- Structure-based functional mechanisms and biotechnology applications of anti-CRISPR proteins.Nature reviews. Molecular cell biology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of type I CRISPR-Cas systems is the presence of Cas3, which contains both the nuclease and helicase activities required for DNA cleavage during interference. In subtype I-D systems, however, the histidine-aspartate (HD) nuclease domain is encoded as part of a Cas10-like large effector complex subunit and the helicase activity in a separate Cas3' subunit, but the functional and mechanistic consequences of this organisation are not currently understood. Here we show that the Sulfolobus islandicus type I-D Cas10d large subunit exhibits an unusual domain architecture consisting of a Cas3-like HD nuclease domain fused to a degenerate polymerase fold and a C-terminal domain structurally similar to Cas11. Crystal structures of Cas10d both in isolation and bound to S. islandicus rod-shaped virus 3 AcrID1 reveal that the anti-CRISPR protein sequesters the large subunit in a non-functional state unable to form a cleavage-competent effector complex. The architecture of Cas10d suggests that the type I-D effector complex is similar to those found in type III CRISPR-Cas systems and that this feature is specifically exploited by phages for anti-CRISPR defence.
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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.