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反CRISPR菌体合作克服CRISPR-Cas免疫力

Mariann Landsberger¹, Sylvain Gandon², Sean Meaden¹

¹ESI and CEC, Biosciences, University of Exeter, Cornwall Campus, Penryn TR10 9EZ, UK.

|July 24, 2018

概括

具有抗CRISPR基因的菌体可以通过合作克服细菌的CRISPR-Cas免疫力,从而导致菌体流行. 较高的细菌免疫力或较弱的抗CRISPR活性需要更多的菌体来引发流行病.

科学领域:

微生物学
遗传学
生态学

背景情况:

菌体 (菌体) 使用抗CRISPR (Acr) 基因对抗细菌CRISPR-Cas适应性免疫系统.
Acr基因部署对菌体复制和流行病学的影响尚不完全理解.

研究的目的:

研究Acr基因如何影响菌体-CRISPR-宿主相互作用和细菌-菌体群体动态.
为了阐明Acr-介导的细菌免疫抑制的流行病学后果.

主要方法:

菌体与细菌相互作用的数学建模.
对细菌CRISPR-Cas耐药性和Acr活性进行分析.
对Acr编码菌体的流行病学转折点的模拟.

主要成果:

具有CRISPR- Cas耐药性的细菌对Acr编码菌体具有部分免疫力.
菌体通常需要合作性感染来克服宿主CRISPR-Cas的防御.
农菌之间的合作可能导致流行病学转折点,从灭绝转变为流行病.
增加的CRISPR- Cas免疫力或降低的Acr有效性需要更高的初始菌体密度以建立流行病.

结论:

菌体Acr系统和细菌CRISPR-Cas免疫之间的相互作用是细菌菌体群动态的关键驱动因素.
通过Acr-phages的合作感染策略对于克服宿主免疫力和建立流行病至关重要.
流行病学转折点受细菌免疫水平的相互作用和菌体抗CRISPR机制的有效性影响.

关键词:

大道效应在CRISPR-Cas 抗CRISPR的方法细菌分叉式流行病学免疫抑制免疫抑制部分电阻菌体临界点

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