Three New Cs for CRISPR: Collateral, Communicate, Cooperate.
Three New Cs for CRISPR: Collateral, Communicate, Cooperate.
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DOI：
10.1016/j.tig.2019.03.009
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发表时间：
2019-06
期刊：
影响因子：
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通讯作者：
Andrew Varble;L. Marraffini
中科院分区：
文献类型：
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作者：
Andrew Varble;L. Marraffini
规则间隔的短回文重复序列（CRISPR）基因座及其相关（cas）基因在原核生物中提供针对入侵的质粒和质粒的保护。通常，从入侵者的基因组捕获短序列，将其整合到CRISPR基因座中，并转录成短RNA，所述短RNA将RNA引导的Cas核酸酶引导至入侵者的核酸以进行降解。该领域的最新工作揭示了CRISPR-Cas机制的意想不到的特征：（i）宿主核酸的附带、非特异性切割;（ii）放大免疫应答的第二信使;和（iii）通过噬菌体编码的抑制剂对CRISPR靶向的免疫抑制。在这里，我们回顾这些新的和令人兴奋的发现。
Clustered regularly interspaced short palindromic repeats (CRISPR) loci and their associated (cas) genes provide protection against invading phages and plasmids in prokaryotes. Typically, short sequences are captured from the genome of the invader, integrated into the CRISPR locus, and transcribed into short RNAs that direct RNA-guided Cas nucleases to the nucleic acids of the invader for their degradation. Recent work in the field has revealed unexpected features of the CRISPR-Cas mechanism: (i) collateral, nonspecific, cleavage of host nucleic acids; (ii) secondary messengers that amplify the immune response; and (iii) immunosuppression of CRISPR targeting by phage-encoded inhibitors. Here, we review these new and exciting findings.