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Mode of Action (MoA)
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abolishes spacer acquisition by the type I-A CRISPR/Cas system.
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Evidence
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Viral Cas4 protein (AcrIA1) was identified as an anti-adaptation factor through plasmid challenge and transformation assays in Sulfolobus islandicus overexpressing both the CRISPR activator Csa3a and a virus-encoded Cas4 from SSV Ragged Hills (SSVRH). Overexpression of AcrIA1 resulted in a near-complete loss of new spacer acquisition, as confirmed by the absence of expanded PCR bands in CRISPR arrays and <1% acquisition efficiency based on high-throughput sequencing. Despite this loss, the remaining spacers retained normal length distribution, indicating that AcrIA1 did not affect spacer size but specifically interfered with acquisition activity. Protospacers from the few acquired spacers lacked the conserved 3′ A/G motif, suggesting interference with motif recognition. These findings indicate that AcrIA1 inhibits the CRISPR-Cas subtype I-A system by suppressing PAM- and motif-dependent spacer acquisition, enabling potential escape of viral DNA from host immunity.
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MoA Category
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unknown
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Subtype(s) of the defence system(s) inhibited by the protein
Defence Subtype
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Sulfolobus islandicus type I-A CRISPR-Cas
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Relevant publication(s)
DOI
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10.1128/jb.00747-18,
10.1016/j.jmb.2023.167996
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Other components of the anti-defence system
Multicomponent System
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-
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Known structure in PDB
PDB ID
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-
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Genome(s) encoding the protein
Protein Source
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Sulfolobus spindle-shaped virus Ragged Hills
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Defence system(s) inhibited by the protein
Defences
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CRISPR-Cas
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View homologs from eukaryotic dsDNA viruses
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