Phages and other mobile genetic elements express anti-CRISPR proteins (Acrs) to protect their genomes from destruction by CRISPR-Cas systems. Acrs usually block the ability of CRISPR-Cas systems to bind or cleave their nucleic acid substrates. Here, we investigate an unusual Acr, AcrIF9, that induces a gain-of-function to a type I-F CRISPR-Cas (Csy) complex, causing it to bind strongly to DNA that lacks both a PAM sequence and sequence complementarity. We show that specific and non-specific dsDNA compete for the same site on the Csy:AcrIF9 complex with rapid exchange, but specific ssDNA appears to still bind through complemetarity to the CRISPR RNA. We also demonstrate that induction of non-specific DNA-binding is a conserved property of diverse AcrIF9 homologues, implying that this activity contributes the biologically relevant function of this Acr family. AcrIF9 provides another example of the surprising variety of mechanisms by which Acrs inhibit CRISPR-Cas systems.

中文翻译：

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抗CRISPR蛋白在CRISPR-Cas复合物中诱导强大的非特异性DNA结合活性

噬菌体和其他可移动遗传元件表达抗CRISPR蛋白（Acrs），以保护其基因组免受CRISPR-Cas系统破坏。Acrs通常会阻止CRISPR-Cas系统结合或切割其核酸底物的能力。在这里，我们研究了一种不寻常的Acr AcrIF9，该Acr诱导了IF CRISPR-Cas（Csy）复合物的功能获得，使其与缺乏PAM序列和序列互补性的DNA牢固结合。我们显示特异性和非特异性dsDNA通过快速交换竞争Csy：AcrIF9复合物上的相同位点，但特异性ssDNA似乎仍通过互补性与CRISPR RNA结合。我们还证明了非特异性DNA结合的诱导是多种AcrIF9同源物的保守特性，暗示该活性有助于该Acr家族的生物学相关功能。AcrIF9提供了令人惊讶的各种机制（通过Acrs抑制CRISPR-Cas系统）的另一个例子。