清脆的
效应器
反式激活crRNA
生物
计算生物学
基因组编辑
Cas9
基因组
质粒
寡核苷酸
细胞生物学
DNA
遗传学
基因
作者
Ning Jia,Dinshaw J. Patel
标识
DOI:10.1038/s41580-021-00371-9
摘要
CRISPR loci and Cas proteins provide adaptive immunity in prokaryotes against invading bacteriophages and plasmids. In response, bacteriophages have evolved a broad spectrum of anti-CRISPR proteins (anti-CRISPRs) to counteract and overcome this immunity pathway. Numerous anti-CRISPRs have been identified to date, which suppress single-subunit Cas effectors (in CRISPR class 2, type II, V and VI systems) and multisubunit Cascade effectors (in CRISPR class 1, type I and III systems). Crystallography and cryo-electron microscopy structural studies of anti-CRISPRs bound to effector complexes, complemented by functional experiments in vitro and in vivo, have identified four major CRISPR–Cas suppression mechanisms: inhibition of CRISPR–Cas complex assembly, blocking of target binding, prevention of target cleavage, and degradation of cyclic oligonucleotide signalling molecules. In this Review, we discuss novel mechanistic insights into anti-CRISPR function that have emerged from X-ray crystallography and cryo-electron microscopy studies, and how these structures in combination with function studies provide valuable tools for the ever-growing CRISPR–Cas biotechnology toolbox, to be used for precise and robust genome editing and other applications.
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