Control of Staphylococcus aureus pathogenicity island excision
Control of Staphylococcus aureus pathogenicity island excision
复制标题
DOI：
10.1111/j.1365-2958.2012.08145.x
复制
发表时间：
2012-09-01
影响因子：
3.6
通讯作者：
Penades, Jose R.
中科院分区：
文献类型：
--
作者：
Mir-Sanchis, Ignacio;Martinez-Rubio, Roser;Penades, Jose R.
金黄色葡萄球菌致病岛（Staphylococcus aureus pathogenicity islands，SaPI）是一组1517 kb的移动的遗传元件，通常携带超抗原毒素和其他毒力因子的基因。它们的移动性的关键特征是通过某些细菌诱导SaPI切除和复制，以及它们有效地粘附到特定的小头噬菌体样感染性颗粒中。以前的工作表明，染色体整合依赖于SaPI编码的重组酶，Int。然而，虽然参与的过程中，Int单独是不足以介导有效的SaPI切除从染色体位点，我们预计，SaPI切除将涉及Xis功能，这可能是编码的辅助噬菌体或由SaPI，本身。在这里，我们报告的情况是后者。大肠杆菌中质粒的体内重组试验表明，SaPI编码的Xis是SaPI attL和attR位点之间重组所绝对需要的，并且这两个位点以及它们的侧翼SaPI序列是SaPI切除所必需的。突变分析表明，Xis是必要的有效的水平SaPI转移到受体菌株。最后，我们表明，主调节SaPI的生命周期，Stl，块的表达int和xis通过结合到启动子区域中存在的反向重复序列，从而控制SaPI切除。
Staphylococcus aureus pathogenicity islands (SaPIs) are a group of related 1517 kb mobile genetic elements that commonly carry genes for superantigen toxins and other virulence factors. The key feature of their mobility is the induction of SaPI excision and replication by certain phages and their efficient encapsidation into specific small-headed phage-like infectious particles. Previous work demonstrated that chromosomal integration depends on the SaPI-encoded recombinase, Int. However, although involved in the process, Int alone was not sufficient to mediate efficient SaPI excision from chromosomal sites, and we expected that SaPI excision would involve an Xis function, which could be encoded by a helper phage or by the SaPI, itself. Here we report that the latter is the case. In vivo recombination assays with plasmids in Escherichia coli demonstrate that SaPI-coded Xis is absolutely required for recombination between the SaPI attL and attR sites, and that both sites, as well as their flanking SaPI sequences, are required for SaPI excision. Mutational analysis reveals that Xis is essential for efficient horizontal SaPI transfer to a recipient strain. Finally, we show that the master regulator of the SaPI life cycle, Stl, blocks expression of int and xis by binding to inverted repeats present in the promoter region, thus controlling SaPI excision.