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更多勾结证据:分枝杆菌噬菌体 Sbash 编码的一种新的前噬菌体介导的病毒防御系统。

More Evidence of Collusion: a New Prophage-Mediated Viral Defense System Encoded by Mycobacteriophage Sbash.

机构信息

Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

出版信息

mBio. 2019 Mar 19;10(2):e00196-19. doi: 10.1128/mBio.00196-19.

DOI:10.1128/mBio.00196-19
PMID:30890613
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6426596/
Abstract

The arms race between bacteria and their bacteriophages profoundly influences microbial evolution. With an estimated 10 phage infections occurring per second, there is strong selection for both bacterial survival and phage coevolution for continued propagation. Many phage resistance systems, including restriction-modification systems, clustered regularly interspaced short palindromic repeat-Cas (CRISPR-Cas) systems, a variety of abortive infection systems, and many others that are not yet mechanistically defined, have been described. Temperate bacteriophages are common and form stable lysogens that are immune to superinfection by the same or closely related phages. However, temperate phages collude with their hosts to confer defense against genomically distinct phages, to the mutual benefit of the bacterial host and the prophage. Prophage-mediated viral systems have been described in phages and phages but are predicted to be widespread throughout the microbial world. Here we describe a new viral defense system in which the mycobacteriophage Sbash prophage colludes with its host to confer highly specific defense against infection by the unrelated mycobacteriophage Crossroads. Sbash genes and are lysogenically expressed and are necessary and sufficient to confer defense against Crossroads but do not defend against any of the closely related phages grouped in subcluster L2. The mapping of Crossroads defense escape mutants shows that genes and are involved in recognition by the Sbash defense system and are proposed to activate a loss in membrane potential mediated by Sbash gp30 and gp31. Viral infection is an ongoing challenge to bacterial survival, and there is strong selection for development or acquisition of defense systems that promote survival when bacteria are attacked by bacteriophages. Temperate phages play central roles in these dynamics through lysogenic expression of genes that defend against phage attack, including those unrelated to the prophage. Few prophage-mediated viral defense systems have been characterized, but they are likely widespread both in phage genomes and in the prophages integrated in bacterial chromosomes.

摘要

细菌与其噬菌体之间的军备竞赛深刻地影响了微生物的进化。据估计,每秒发生 10 次噬菌体感染,因此细菌的生存和噬菌体的共同进化对于持续传播都有强烈的选择压力。已经描述了许多噬菌体抗性系统,包括限制修饰系统、成簇规律间隔短回文重复 CRISPR-Cas(CRISPR-Cas)系统、多种流产感染系统,以及许多其他尚未在机制上定义的系统。温和噬菌体很常见,形成稳定的溶原菌,对同一或密切相关的噬菌体的再次感染具有免疫力。然而,温和噬菌体与它们的宿主勾结,赋予宿主防御与基因组不同的噬菌体的能力,这对细菌宿主和原噬菌体都是有利的。已经在噬菌体和噬菌体中描述了原噬菌体介导的病毒系统,但预计它们在微生物世界中广泛存在。在这里,我们描述了一个新的病毒防御系统,其中分枝杆菌噬菌体 Sbash 原噬菌体与它的宿主勾结,赋予宿主针对不相关的分枝杆菌噬菌体 Crossroads 的高度特异性防御。Sbash 基因和在溶原状态下表达,是赋予对 Crossroads 防御所必需且充分的,但不能防御任何属于亚群 L2 的密切相关的噬菌体。Crossroads 防御逃逸突变体的作图表明,基因和参与 Sbash 防御系统的识别,并提出激活 Sbash gp30 和 gp31 介导的膜电位丧失。病毒感染是细菌生存的持续挑战,因此强烈选择开发或获得防御系统,以促进细菌在受到噬菌体攻击时的生存。温和噬菌体通过溶原状态下表达防御噬菌体攻击的基因,在这些动态中起着核心作用,包括与原噬菌体无关的基因。已经描述了少数原噬菌体介导的病毒防御系统,但它们在噬菌体基因组中和整合在细菌染色体中的原噬菌体中都可能广泛存在。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/7b9b784381ea/mBio.00196-19-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/a271792441ec/mBio.00196-19-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/e022e8af3e43/mBio.00196-19-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/124096721d33/mBio.00196-19-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/64ed67700883/mBio.00196-19-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/59ded0aefa73/mBio.00196-19-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/8e27aaee6581/mBio.00196-19-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/e87cda1f4bb6/mBio.00196-19-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/01772383c2cd/mBio.00196-19-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/7b9b784381ea/mBio.00196-19-f0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/a271792441ec/mBio.00196-19-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/e022e8af3e43/mBio.00196-19-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/124096721d33/mBio.00196-19-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/64ed67700883/mBio.00196-19-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/59ded0aefa73/mBio.00196-19-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/8e27aaee6581/mBio.00196-19-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/e87cda1f4bb6/mBio.00196-19-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/01772383c2cd/mBio.00196-19-f0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0ea5/6426596/7b9b784381ea/mBio.00196-19-f0009.jpg

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