Suppr超能文献

辅助性黏粒噬菌体干扰中致病岛的趋同进化。

Convergent evolution of pathogenicity islands in helper cos phage interference.

作者信息

Carpena Nuria, Manning Keith A, Dokland Terje, Marina Alberto, Penadés José R

机构信息

Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, UK Departamento de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad CEU Cardenal Herrera, 46113 Moncada, Valencia, Spain.

Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2016 Nov 5;371(1707). doi: 10.1098/rstb.2015.0505.

Abstract

Staphylococcus aureus pathogenicity islands (SaPIs) are phage satellites that exploit the life cycle of their helper phages for their own benefit. Most SaPIs are packaged by their helper phages using a headful (pac) packaging mechanism. These SaPIs interfere with pac phage reproduction through a variety of strategies, including the redirection of phage capsid assembly to form small capsids, a process that depends on the expression of the SaPI-encoded cpmA and cpmB genes. Another SaPI subfamily is induced and packaged by cos-type phages, and although these cos SaPIs also block the life cycle of their inducing phages, the basis for this mechanism of interference remains to be deciphered. Here we have identified and characterized one mechanism by which the SaPIs interfere with cos phage reproduction. This mechanism depends on a SaPI-encoded gene, ccm, which encodes a protein involved in the production of small isometric capsids, compared with the prolate helper phage capsids. As the Ccm and CpmAB proteins are completely unrelated in sequence, this strategy represents a fascinating example of convergent evolution. Moreover, this result also indicates that the production of SaPI-sized particles is a widespread strategy of phage interference conserved during SaPI evolution.This article is part of the themed issue 'The new bacteriology'.

摘要

金黄色葡萄球菌致病岛(SaPIs)是噬菌体卫星,它们利用辅助噬菌体的生命周期来为自身谋利。大多数SaPIs由其辅助噬菌体通过满头部(pac)包装机制进行包装。这些SaPIs通过多种策略干扰pac噬菌体的繁殖,包括将噬菌体衣壳组装重定向以形成小衣壳,这一过程依赖于SaPI编码的cpmA和cpmB基因的表达。另一个SaPI亚家族由cos型噬菌体诱导并包装,尽管这些cos SaPIs也会阻断其诱导噬菌体的生命周期,但这种干扰机制的基础仍有待阐明。在这里,我们确定并描述了SaPIs干扰cos噬菌体繁殖的一种机制。该机制依赖于一个SaPI编码基因ccm,它编码一种参与产生小等轴衣壳的蛋白质,与细长的辅助噬菌体衣壳不同。由于Ccm和CpmAB蛋白在序列上完全不相关,这种策略代表了趋同进化的一个引人入胜的例子。此外,这一结果还表明,产生SaPI大小的颗粒是在SaPI进化过程中保守的一种广泛存在的噬菌体干扰策略。本文是主题为“新细菌学”的特刊的一部分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2d11/5052747/ff46baaff82f/rstb20150505-g1.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验