Skirball Institute for Biomolecular Medicine, New York University School of Medicine, Departments of Medicine and Microbiology, 540 First Ave., New York, NY 10016, USA.
Skirball Institute for Biomolecular Medicine, New York University School of Medicine, Departments of Medicine and Microbiology, 540 First Ave., New York, NY 10016, USA.
Curr Opin Microbiol. 2017 Aug;38:197-204. doi: 10.1016/j.mib.2017.08.001. Epub 2017 Nov 1.
The staphylococcal pathogenicity islands (SaPIs) are highly mobile 15kb genomic islands that carry superantigen genes and other virulence factors and are mobilized by helper phages. Helper phages counteract the SaPI repressor to induce the SaPI replication cycle, resulting in encapsidation in phage like particles, enabling high frequency transfer. The SaPIs split from a protophage lineage in the distant past, have evolved a variety of novel and salient features, and have become an invaluable component of the staphylococcal genome. This review focuses on recent studies describing three different mechanisms of SaPI interference with helper phage reproduction and other studies demonstrating that helper phage mutations to resistance against this interference impact phage evolution. Also described are recent results showing that SaPIs contribute in a major way to lateral transfer of host genes as well as enabling their own transfer. SaPI-like elements, readily identifiable in the bacterial genome, are widespread throughout the Gram-positive cocci, though functionality has thus far been demonstrated for only a single one of these.
葡萄球菌致病性岛(SaPIs)是高度移动的 15kb 基因组岛,携带超抗原基因和其他毒力因子,并由辅助噬菌体进行移动。辅助噬菌体对抗 SaPI 阻遏物以诱导 SaPI 复制周期,导致类似噬菌体颗粒的包裹,从而实现高频转移。SaPIs 从远古时期的原噬菌体谱系中分裂出来,已经进化出多种新颖而显著的特征,并成为葡萄球菌基因组的宝贵组成部分。本综述重点介绍了最近描述 SaPI 干扰辅助噬菌体繁殖的三种不同机制的研究,以及证明辅助噬菌体突变以抵抗这种干扰会影响噬菌体进化的其他研究。还描述了最近的结果,表明 SaPIs 主要有助于宿主基因的水平转移,并使其自身转移。SaPI 样元件在细菌基因组中很容易识别,广泛存在于革兰氏阳性球菌中,但迄今为止仅证明了其中一个的功能。