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AcrIIC5的结构变异通过不同的结合接口抑制Cas9

Sung-Hyun Hong¹, So Young An¹, Changkon Park¹

¹Department of Agricultural Biotechnology, Seoul National University, Seoul 08826, South Korea.

Structure (London, England : 1993)

|January 18, 2025

概括

细菌的CRISPR-Cas系统受到反CRISPR蛋白质的保护. 这项研究揭示了AcrIIC5蛋白折叠变异如何允许各种接口抑制Cas9,帮助菌体适应.

科学领域:

分子生物学分子生物学
结构生物学结构生物学
遗传学遗传学是一个

背景情况:

克里斯普尔-卡斯系统为细菌提供了对外来核酸的适应性免疫力.
菌体利用抗CRISPR (Acr) 蛋白质在感染期间抵消CRISPR-Cas防御.
作为一种Cas9抑制剂的AcrIIC5,在它的正确基因组中显示出显著的结构变异.

研究的目的:

研究AcrIIC5结构变异对Cas9抑制的影响.
通过AcrIIC5的ortologs识别差异性Cas9抑制的关键残留物和机制.

主要方法:

在AcrIIC5的结构上进行了对比 (AcrIIC5_Smu和AcrIIC5_Nch).
基因突变和生物化学测试以评估Cas9抑制.
用AlphaFold2预测来建模蛋白质结构和相互作用.

主要成果:

在 AcrIIC5 的折叠变化与螺旋区域的内相关.
关键的残留物对Cas9抑制至关重要,通过突变发生症被确定.
由于结构变异,AcrIIC5正位器使用不同的结合接口来抑制向Cas9.

结论:

亚克蛋白已经进化了多种结构变体,以调节它们与Cas9.9的接口.
这些结构性适应增强了菌体适应能力,对抗不断演变的Cas9防御.
了解这些变异可以了解菌体与宿主相互作用以及CRISPR-Cas系统的演变.

关键词:

这就是AcrIIC5的意思.这是一个反-CRISPR.抑制机制是一种抑制机制.解决方案结构解决方案结构类型II-C Cas9 类型的

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