“中毒性休克綜合征”是一種罕見的、潛在致命的疾病,，可由葡萄球菌毒素的釋放引起,。
有毒顆粒是由被稱為“致病性島”的離散遺傳單元編碼的，這些“致病性島”被動地存在于宿主的染色體中,，受普遍性抑制因子Stl的控制,，除非被一個輔助噬菌體激發(fā)?，F(xiàn)在研究發(fā)現(xiàn),，來自輔助噬菌體80α的并非必要的,、特定的蛋白對“致病性島”的“去抑制”負責，從而為其活化的第一步提供機制,。
這個過程中所涉及的蛋白是“兼職者”,，因為它們有兩個不同的、在遺傳上有各自鮮明特征的活性,。各種不同的“致病性島”通過一個引人注目的演化適應性變化,，選擇完全不相關的噬菌體蛋白來幫助它們活化。 (生物谷Bioon.com)
生物谷推薦原文出處：
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.
