An insight into staphylococcal pathogenicity island-mediated interference with phage late gene transcription.

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
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引用次数: 3

Abstract

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.

洞察葡萄球菌致病性岛介导的干扰噬菌体晚期基因转录。
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。
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