The Type 2 dUTPase of Bacteriophage φNM1 Initiates Mobilization of Staphylococcus aureus Bovine Pathogenicity Island 1
The Type 2 dUTPase of Bacteriophage φNM1 Initiates Mobilization of Staphylococcus aureus Bovine Pathogenicity Island 1
复制标题
DOI：
10.1016/j.jmb.2015.11.009
复制
发表时间：
2016-01-16
影响因子：
5.6
通讯作者：
Dokland, Terje
中科院分区：
文献类型：
--
作者：
Hill, Rosanne L. L.;Dokland, Terje
金黄色葡萄球菌致病岛（Staphylococcus aureus pathogenicity islands，SaPI）是由特定的辅助因子动员的遗传元件。动员的初始步骤是通过噬菌体蛋白与SaPI主阻遏物StI的相互作用使SaPI去阻遏。Stl蛋白在不同的SaPI之间是高度不同的，并且响应于不同的噬菌体编码的去阻遏物。一种这样的SaPI，SaPlbov 1，被噬菌体80 α（Dut（80 α））及其噬菌体phi（11）同源物Dut（11）的dUTR（Dut）去阻遏。我们以前表明，SaPlbov 1也可以被噬菌体phi NM 1动员，即使它的dut基因与80 a的dut基因不同源。在这里，我们表明phi NM 1 dutencode 2型dUTR（Dut（NM 1）），它具有a-螺旋结构，不同于Dut（80 α）的1型三聚体β-折叠结构。dut（NM 1）的缺失消除了phi NM 1动员SaPlbov 1的能力。与Dut（80 α）一样，Dut（NM 1）在体内和体外与SaPlbov 1 Stl形成直接相互作用，导致dUTR活性和StI从其靶DNA释放的抑制。这项工作提供了新的见解的不同机制的遗传动员在S。金黄色。(C)2015爱思唯尔有限公司版权所有。
Staphylococcus aureus pathogenicity islands (SaPIs) are genetic elements that are mobilized by specific helper phages. The initial step in mobilization is the derepression of the SaPI by the interaction of a phage protein with the SaPI master repressor StI. Stl proteins are highly divergent between different SaPIs and respond to different phage-encoded derepressors. One such SaPI, SaPlbov1, is derepressed by the dUTPase (Dut) of bacteriophage 80 alpha (Dut(80 alpha)) and its phage phi(11) homolog, Dut(11). We previously showed that SaPlbov1 could also be mobilized by phage phi NM1, even though its dut gene is not homologous with that of 80a. Here, we show that phi NM1 dutencodes a type 2 dUTPase (Dut(NM1)), which has an a-helical structure that is distinct from the type 1 trimeric, beta-sheet structure of Dut(80 alpha). Deletion of dut(NM1) abolishes the ability of phi NM1 to mobilize SaPlbov1. Like Dut(80 alpha), Dut(NM1) forms a direct interaction with SaPlbov1 Stl both in vivo and in vitro, leading to inhibition of the dUTPase activity and StI release from its target DNA. This work provides novel insights into the diverse mechanisms of genetic mobilization in S. aureus. (C) 2015 Elsevier Ltd. All rights reserved.