CRISPR/Cas9介导的噬菌体抗性不受噬菌体T4的DNA修饰影响。

CRISPR/Cas9-mediated phage resistance is not impeded by the DNA modifications of phage T4.

作者信息

Yaung Stephanie J, Esvelt Kevin M, Church George M

机构信息

Wyss Institute for Biologically Inspired Engineering, Harvard Medical School, Boston, Massachusetts, United States of America; Department of Genetics, Harvard Medical School, Boston, Massachusetts, United States of America; Program in Medical Engineering & Medical Physics, Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.

Wyss Institute for Biologically Inspired Engineering, Harvard Medical School, Boston, Massachusetts, United States of America.

出版信息

PLoS One. 2014 Jun 2;9(6):e98811. doi: 10.1371/journal.pone.0098811. eCollection 2014.

Abstract

Bacteria rely on two known DNA-level defenses against their bacteriophage predators: restriction-modification and Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-CRISPR-associated (Cas) systems. Certain phages have evolved countermeasures that are known to block endonucleases. For example, phage T4 not only adds hydroxymethyl groups to all of its cytosines, but also glucosylates them, a strategy that defeats almost all restriction enzymes. We sought to determine whether these DNA modifications can similarly impede CRISPR-based defenses. In a bioinformatics search, we found naturally occurring CRISPR spacers that potentially target phages known to modify their DNA. Experimentally, we show that the Cas9 nuclease from the Type II CRISPR system of Streptococcus pyogenes can overcome a variety of DNA modifications in Escherichia coli. The levels of Cas9-mediated phage resistance to bacteriophage T4 and the mutant phage T4 gt, which contains hydroxymethylated but not glucosylated cytosines, were comparable to phages with unmodified cytosines, T7 and the T4-like phage RB49. Our results demonstrate that Cas9 is not impeded by N6-methyladenine, 5-methylcytosine, 5-hydroxymethylated cytosine, or glucosylated 5-hydroxymethylated cytosine.

摘要

细菌依靠两种已知的针对噬菌体捕食者的DNA水平防御机制:限制修饰和成簇规律间隔短回文重复序列(CRISPR)-CRISPR相关(Cas)系统。某些噬菌体已经进化出了已知的可阻断核酸内切酶的对策。例如,噬菌体T4不仅会在其所有胞嘧啶上添加羟甲基基团,还会使其糖基化,这一策略几乎能击败所有限制酶。我们试图确定这些DNA修饰是否同样会阻碍基于CRISPR的防御机制。在一次生物信息学搜索中,我们发现了天然存在的CRISPR间隔序列,其可能靶向已知会修饰自身DNA的噬菌体。通过实验,我们表明化脓性链球菌II型CRISPR系统中的Cas9核酸酶能够克服大肠杆菌中的多种DNA修饰。Cas9介导的对噬菌体T4和突变噬菌体T4 gt(其胞嘧啶含有羟甲基化但未糖基化)的噬菌体抗性水平,与胞嘧啶未修饰的噬菌体T7和T4样噬菌体RB49相当。我们的结果表明,Cas9不受N6-甲基腺嘌呤、5-甲基胞嘧啶、5-羟甲基化胞嘧啶或糖基化的5-羟甲基化胞嘧啶的阻碍。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5c5d/4041780/8a393bf52356/pone.0098811.g001.jpg

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