“中毒性休克综合征”是一种罕见的、潜在致命的疾病，可由葡萄球菌毒素的释放引起。
有毒颗粒是由被称为“致病性岛”的离散遗传单元编码的，这些“致病性岛”被动地存在于宿主的染色体中，受普遍性抑制因子Stl的控制，除非被一个辅助噬菌体激发。现在研究发现，来自辅助噬菌体80α的并非必要的、特定的蛋白对“致病性岛”的“去抑制”负责，从而为其活化的第一步提供机制。
这个过程中所涉及的蛋白是“兼职者”，因为它们有两个不同的、在遗传上有各自鲜明特征的活性。各种不同的“致病性岛”通过一个引人注目的演化适应性变化，选择完全不相关的噬菌体蛋白来帮助它们活化。 (生物谷Bioon.com)
生物谷推荐原文出处：
Nature doi:10.1038/nature09065
Moonlighting bacteriophage proteins derepress staphylococcal pathogenicity islands
María ángeles Tormo-Más1Search Ignacio Mir1Search Archana Shrestha2 Sandra M. Tallent2Search Susana Campoy3 í?igo Lasa4 Jordi Barbé3 Richard P. Novick5 Gail E. Christie2 José R. Penadés
Staphylococcal superantigen-carrying pathogenicity islands (SaPIs) are discrete, chromosomally integrated units of ~15 kilobases that are induced by helper phages to excise and replicate. SaPI DNA is then efficiently encapsidated in phage-like infectious particles, leading to extremely high frequencies of intra- as well as intergeneric transfer1, 2, 3. In the absence of helper phage lytic growth, the island is maintained in a quiescent prophage-like state by a global repressor, Stl, which controls expression of most of the SaPI genes4. Here we show that SaPI derepression is effected by a specific, non-essential phage protein that binds to Stl, disrupting the Stl–DNA complex and thereby initiating the excision-replication-packaging cycle of the island. Because SaPIs require phage proteins to be packaged5, 6, this strategy assures that SaPIs will be transferred once induced. Several different SaPIs are induced by helper phage 80α and, in each case, the SaPI commandeers a different non-essential phage protein for its derepression. The highly specific interactions between different SaPI repressors and helper-phage-encoded antirepressors represent a remarkable evolutionary adaptation involved in pathogenicity island mobilization.
