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原间隔识别基序:混合身份和功能多样性。

Protospacer recognition motifs: mixed identities and functional diversity.

机构信息

Archaea Centre, Department of Biology, University of Copenhagen, Copenhagen, Denmark.

出版信息

RNA Biol. 2013 May;10(5):891-9. doi: 10.4161/rna.23764. Epub 2013 Feb 12.

DOI:10.4161/rna.23764
PMID:23403393
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3737346/
Abstract

Protospacer adjacent motifs (PAMs) were originally characterized for CRISPR-Cas systems that were classified on the basis of their CRISPR repeat sequences. A few short 2-5 bp sequences were identified adjacent to one end of the protospacers. Experimental and bioinformatical results linked the motif to the excision of protospacers and their insertion into CRISPR loci. Subsequently, evidence accumulated from different virus- and plasmid-targeting assays, suggesting that these motifs were also recognized during DNA interference, at least for the recently classified type I and type II CRISPR-based systems. The two processes, spacer acquisition and protospacer interference, employ different molecular mechanisms, and there is increasing evidence to suggest that the sequence motifs that are recognized, while overlapping, are unlikely to be identical. In this article, we consider the properties of PAM sequences and summarize the evidence for their dual functional roles. It is proposed to use the terms protospacer associated motif (PAM) for the conserved DNA sequence and to employ spacer acqusition motif (SAM) and target interference motif (TIM), respectively, for acquisition and interference recognition sites.

摘要

原间隔相邻基序 (PAMs) 最初是根据 CRISPR 重复序列对 CRISPR-Cas 系统进行分类时确定的。在原间隔区的一端附近鉴定出了一些短的 2-5bp 序列。实验和生物信息学结果将该基序与原间隔区的切除及其插入 CRISPR 基因座联系起来。随后,来自不同病毒和质粒靶向测定的证据表明,这些基序在 DNA 干扰过程中也被识别,至少对于最近分类的基于 I 型和 II 型 CRISPR 的系统是如此。间隔区获取和原间隔区干扰这两个过程采用不同的分子机制,越来越多的证据表明,虽然识别的序列基序重叠,但不太可能相同。在本文中,我们考虑了 PAM 序列的特性,并总结了它们双重功能作用的证据。建议将保守的 DNA 序列称为原间隔区相关基序 (PAM),并分别将获取和干扰识别位点称为间隔区获取基序 (SAM) 和目标干扰基序 (TIM)。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/345a6f541638/rna-10-891-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/78f4a0c724d0/rna-10-891-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/6252687b5250/rna-10-891-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/345a6f541638/rna-10-891-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/78f4a0c724d0/rna-10-891-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/6252687b5250/rna-10-891-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b17/3737346/345a6f541638/rna-10-891-g3.jpg

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Front Cell Infect Microbiol. 2025 May 30;15:1588446. doi: 10.3389/fcimb.2025.1588446. eCollection 2025.
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