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Abstract
The high-resolution structure of Aca3 provides insight into its function in regulating anti-CRISPR expression.
- Aca3 selectively binds to specific DNA sequences located upstream of its associated anti-CRISPR gene, AcrIIC1.
- The interaction involves key structural features, specifically helix-turn-helix motifs, which are crucial for binding to the promoter.
- Mutational analysis indicates that alterations in these motifs disrupt the ability of Aca3 to engage with DNA.
- These findings contribute to understanding how bacteriophages can influence bacterial immune responses by controlling anti-CRISPR gene expression.
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