Pirating conserved phage mechanisms promotes promiscuous staphylococcal pathogenicity island transfer
Pirating conserved phage mechanisms promotes promiscuous staphylococcal pathogenicity island transfer
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DOI：
10.7554/elife.26487.001
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发表时间：
2017-08-08
期刊：
影响因子：
7.7
通讯作者：
Penades, Jose R.
中科院分区：
文献类型：
--
作者：
Bowring, Janine;Neamah, Maan M.;Penades, Jose R.
以保守和基本的过程为目标是对抗敌人的成功策略。值得注意的是，临床上重要的金黄色葡萄球菌致病性岛（SaPIs）使用这种策略在自然界中传播。在sapi编码的主抑制因子Stl的控制下，sapi被动地驻留在宿主染色体上。据推测，SaPI的去抑制是由与Stl结合的特定噬菌体蛋白影响的，从而启动SaPI周期。不同的sapl编码不同的Stl抑制因子，因此每个都针对特定的噬菌体蛋白进行去抑制。拓宽这一狭窄的视野，我们在这里报告了sapl通过靶向保守的噬菌体机制来确保它们的混杂转移。这是因为SaPI Stl抑制因子获得了不同的结构域来与不同噬菌体编码的不相关蛋白相互作用，但在所有情况下都执行相同的保守功能。这种优雅的策略允许SaPI在属内和属间转移，突出了这些元素作为自然界最迷人的亚细胞寄生虫之一。
Targeting conserved and essential processes is a successful strategy to combat enemies. Remarkably, the clinically important Staphylococcus aureus pathogenicity islands (SaPIs) use this tactic to spread in nature. SaPls reside passively in the host chromosome, under the control of the SaPI-encoded master repressor, Stl. It has been assumed that SaPI de-repression is effected by specific phage proteins that bind to Stl, initiating the SaPI cycle. Different SaPls encode different Stl repressors, so each targets a specific phage protein for its de-repression. Broadening this narrow vision, we report here that SaPls ensure their promiscuous transfer by targeting conserved phage mechanisms. This is accomplished because the SaPI Stl repressors have acquired different domains to interact with unrelated proteins, encoded by different phages, but in all cases performing the same conserved function. This elegant strategy allows intra- and inter-generic SaPI transfer, highlighting these elements as one of nature's most fascinating subcellular parasites.