PDF(Pubmed)
Abstract：
Staphylococcus aureus is an important human pathogen, and the prevalence of antibiotic resistance is a major public health concern. The evolution of pathogenicity and resistance in S. aureus often involves acquisition of mobile genetic elements (MGEs). Bacteriophages play an especially important role, since transduction represents the main mechanism for horizontal gene transfer. S. aureus pathogenicity islands (SaPIs), including SaPI1, are MGEs that carry genes encoding virulence factors, and are mobilized at high frequency through interactions with specific \"helper\" bacteriophages, such as 80α, leading to packaging of the SaPI genomes into virions made from structural proteins supplied by the helper. Among these structural proteins is the portal protein, which forms a ring-like portal at a fivefold vertex of the capsid, through which the DNA is packaged during virion assembly and ejected upon infection of the host. We have used high-resolution cryo-electron microscopy to determine structures of the S. aureus bacteriophage 80α portal itself, produced by overexpression, and in situ in the empty and full SaPI1 virions, and show how the portal interacts with the capsid. These structures provide a basis for understanding portal and capsid assembly and the conformational changes that occur upon DNA packaging and ejection.
摘要：
金黄色葡萄球菌是一种重要的人类病原菌，抗生素耐药性的流行是一个主要的公共卫生问题。金黄色葡萄球菌中致病性和抗性的进化通常涉及可移动遗传元件(MGE)的获得。噬菌体发挥着特别重要的作用,因为转导代表了水平基因转移的主要机制。金黄色葡萄球菌致病性岛(SaPIs)，包括SaPI1，是携带编码毒力因子的基因的MGE，并通过与特定的“辅助”噬菌体相互作用以高频率动员，例如80α，导致将SaPI基因组包装到由助手提供的结构蛋白制成的病毒体中。这些结构蛋白是门静脉蛋白，在衣壳的五倍顶点处形成一个环状入口，DNA在病毒体组装过程中被包装，并在感染宿主时被排出。我们已经使用高分辨率低温电子显微镜来确定金黄色葡萄球菌噬菌体80α门静脉本身的结构，由过度表达产生，在空而满的SaPI1病毒体中，并显示门户如何与衣壳交互。这些结构为理解门户和衣壳组装以及在DNA包装和排出时发生的构象变化提供了基础。
