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靶向温和噬菌体会导致I型CRISPR–Cas系统丢失
2020-01-29 16:32

英国埃克塞特大学Edze R. Westra、Clare Rollie、Anne Chevallereau等研究人员合作发现,靶向温和噬菌体会导致I型CRISPR–Cas系统丢失。2020年1月22日,国际知名学术期刊《自然》发表了这一成果。

研究人员证明,当受到野生型温和噬菌体(可能会引起溶原性)的攻击时,I型CRISPR–Cas免疫系统无法消除细菌群体中的噬菌体。此外,研究人员的数据表明,在这种情况下,由于间隔子与整合的噬菌体序列(原噬菌体)不完全匹配所引起的严重的免疫病理学作用,CRISPR – Cas免疫系统对宿主具有不良适应性。除非噬菌体携带抑制宿主免疫系统的抗CRISPR(acr)基因,否则这些适应会导致细菌群体中CRISPR–Cas的丢失。使用生物信息学,研究人员表明这种不完善的靶向很可能在自然界频繁发生。这些发现有助于解释CRISPR–Cas免疫系统在细菌内部和细菌之间的分布不均,并突出了在这种情况下噬菌体编码的acr基因对噬菌体和宿主的强大选择性。
 
据了解,在感染宿主后,感染细菌的温和病毒(即噬菌体)进入溶菌或溶原循环。前者导致细菌细胞裂解和噬菌体释放(导致水平传播),而溶原性的特征是噬菌体整合入宿主基因组和休眠(导致垂直传播)。以往共培养实验使用的细菌和温和噬菌体的突变体被锁定在裂解周期中,并表明CRISPR–Cas系统可以有效消除入侵的噬菌体。
 
附:英文原文

Title: Targeting of temperate phages drives loss of type I CRISPR–Cas systems

Author: Clare Rollie, Anne Chevallereau, Bridget N. J. Watson, Te-yuan Chyou, Olivier Fradet, Isobel McLeod, Peter C. Fineran, Chris M. Brown, Sylvain Gandon, Edze R. Westra

Issue&Volume: 2020-01-22

Abstract: On infection of their host, temperate viruses that infect bacteria (bacteriophages; hereafter referred to as phages) enter either a lytic or a lysogenic cycle. The former results in lysis of bacterial cells and phage release (resulting in horizontal transmission), whereas lysogeny is characterized by the integration of the phage into the host genome, and dormancy (resulting in vertical transmission)1. Previous co-culture experiments using bacteria and mutants of temperate phages that are locked in the lytic cycle have shown that CRISPR–Cas systems can efficiently eliminate the invading phages2,3. Here we show that, when challenged with wild-type temperate phages (which can become lysogenic), type I CRISPR–Cas immune systems cannot eliminate the phages from the bacterial population. Furthermore, our data suggest that, in this context, CRISPR–Cas immune systems are maladaptive to the host, owing to the severe immunopathological effects that are brought about by imperfect matching of spacers to the integrated phage sequences (prophages). These fitness costs drive the loss of CRISPR–Cas from bacterial populations, unless the phage carries anti-CRISPR (acr) genes that suppress the immune system of the host. Using bioinformatics, we show that this imperfect targeting is likely to occur frequently in nature. These findings help to explain the patchy distribution of CRISPR–Cas immune systems within and between bacterial species, and highlight the strong selective benefits of phage-encoded acr genes for both the phage and the host under these circumstances.

DOI: 10.1038/s41586-020-1936-2

Source: https://www.nature.com/articles/s41586-020-1936-2

Nature:《自然》,创刊于1869年。隶属于施普林格·自然出版集团,最新IF:43.07
官方网址:http://www.nature.com/
投稿链接:http://www.nature.com/authors/submit_manuscript.html


本期文章:《自然》:Online/在线发表

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