洞察葡萄球菌致病性岛介导的干扰噬菌体晚期基因转录。

Bacteriophage Pub Date : 2015-06-11 eCollection Date: 2015-04-01 DOI:10.1080/21597081.2015.1028608
Geeta Ram, John Chen, Hope F Ross, Richard P Novick
{"title":"洞察葡萄球菌致病性岛介导的干扰噬菌体晚期基因转录。","authors":"Geeta Ram,&nbsp;John Chen,&nbsp;Hope F Ross,&nbsp;Richard P Novick","doi":"10.1080/21597081.2015.1028608","DOIUrl":null,"url":null,"abstract":"<p><p>Staphylococcal pathogenicity islands (SaPIs) are ∼15 kb chromosomally located mobile elements that parasitize \"helper\" phages which provide a de-repressor protein plus virion and lysis proteins which enable the release of infectious SaPI particles in very high titers. All SaPIs interfere with the reproduction of their helper phages, using 3 different mechanisms. The logic of SaPI reproduction requires that these interference mechanisms do not totally block phage production, as this would be lethal for them as well as for the phage. The discovery of 2 SaPI2 proteins that totally block phage 80 by interfering with late phage transcription was inconsistent with this principle and led to the discovery of a third protein that binds to one of the interference proteins and modulates its activity, thus preventing complete inhibition of the phage. These systems permit the SaPIs to engage in horizontal transfer of unlinked chromosomal genes as well as their own.</p>","PeriodicalId":8686,"journal":{"name":"Bacteriophage","volume":"5 2","pages":"e1028608"},"PeriodicalIF":0.0000,"publicationDate":"2015-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/21597081.2015.1028608","citationCount":"3","resultStr":"{\"title\":\"An insight into staphylococcal pathogenicity island-mediated interference with phage late gene transcription.\",\"authors\":\"Geeta Ram,&nbsp;John Chen,&nbsp;Hope F Ross,&nbsp;Richard P Novick\",\"doi\":\"10.1080/21597081.2015.1028608\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Staphylococcal pathogenicity islands (SaPIs) are ∼15 kb chromosomally located mobile elements that parasitize \\\"helper\\\" phages which provide a de-repressor protein plus virion and lysis proteins which enable the release of infectious SaPI particles in very high titers. All SaPIs interfere with the reproduction of their helper phages, using 3 different mechanisms. The logic of SaPI reproduction requires that these interference mechanisms do not totally block phage production, as this would be lethal for them as well as for the phage. The discovery of 2 SaPI2 proteins that totally block phage 80 by interfering with late phage transcription was inconsistent with this principle and led to the discovery of a third protein that binds to one of the interference proteins and modulates its activity, thus preventing complete inhibition of the phage. These systems permit the SaPIs to engage in horizontal transfer of unlinked chromosomal genes as well as their own.</p>\",\"PeriodicalId\":8686,\"journal\":{\"name\":\"Bacteriophage\",\"volume\":\"5 2\",\"pages\":\"e1028608\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-06-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1080/21597081.2015.1028608\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Bacteriophage\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/21597081.2015.1028608\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2015/4/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Bacteriophage","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/21597081.2015.1028608","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/4/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 3

摘要

葡萄球菌致病性岛(SaPIs)是位于约15 kb染色体上的可移动元件,寄生在“辅助”噬菌体上,提供去抑制蛋白以及病毒粒子和裂解蛋白,使感染性SaPI颗粒能够以非常高的滴度释放。所有SaPIs都通过3种不同的机制干扰其辅助噬菌体的繁殖。SaPI繁殖的逻辑要求这些干扰机制不能完全阻断噬菌体的产生,因为这对它们和噬菌体都是致命的。通过干扰晚期噬菌体转录完全阻断噬菌体80的2种SaPI2蛋白的发现与这一原理不一致,并导致发现第三种蛋白与其中一种干扰蛋白结合并调节其活性,从而阻止对噬菌体的完全抑制。这些系统允许sapi参与非连锁染色体基因及其自身基因的水平转移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
An insight into staphylococcal pathogenicity island-mediated interference with phage late gene transcription.

Staphylococcal pathogenicity islands (SaPIs) are ∼15 kb chromosomally located mobile elements that parasitize "helper" phages which provide a de-repressor protein plus virion and lysis proteins which enable the release of infectious SaPI particles in very high titers. All SaPIs interfere with the reproduction of their helper phages, using 3 different mechanisms. The logic of SaPI reproduction requires that these interference mechanisms do not totally block phage production, as this would be lethal for them as well as for the phage. The discovery of 2 SaPI2 proteins that totally block phage 80 by interfering with late phage transcription was inconsistent with this principle and led to the discovery of a third protein that binds to one of the interference proteins and modulates its activity, thus preventing complete inhibition of the phage. These systems permit the SaPIs to engage in horizontal transfer of unlinked chromosomal genes as well as their own.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
期刊最新文献
Testing a proposed paradigm shift in analysis of phage DNA packaging Fecal microbiota transplantation to fight Clostridium difficile infections and other intestinal diseases Félix Hubert d'Herelle (1873–1949): History of a scientific mind My scientific life Structural proteins of Enterococcus faecalis bacteriophage ϕEf11
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1