德國杜伊斯堡-埃森大學(xué)(University Duisburg-Essen)教授Peter Bayer和Anja Matena和他們來自蘇格蘭的同事們?nèi)缃褡R破了卵菌(oomycete)感染它們宿主的策略,。相關(guān)研究結(jié)果發(fā)表在美國著名期刊PNAS上,。
卵菌中很多物種是寄生菌，這些看似無害的微動物(animalcule)能夠?qū)е戮薮蟮慕?jīng)濟(jì)損失,，比如致病疫霉(Phytophthora infestans)就是其中的一個代表,。致病疫霉是一種導(dǎo)致馬鈴薯疫病的致病性卵菌,，而且在1845年，它導(dǎo)致愛爾蘭發(fā)生大饑荒,。直到現(xiàn)在,，這種有機(jī)體仍然給全世界種植業(yè)帶來相當(dāng)于上百萬美元的農(nóng)作物損失。然而,，卵菌能夠攻擊和感染的對象不僅是植物,，而且也包括動物以及在少數(shù)情況下還包括人類。因此,，卵菌和它們的傳播方式激起科學(xué)家的濃厚興趣,。
來自“結(jié)構(gòu)與醫(yī)學(xué)生化”研究小組的科學(xué)家與來自蘇格蘭阿伯丁大學(xué)和鄧迪大學(xué)的同事們進(jìn)行合作研究，并破解了卵菌刺入它們的宿主細(xì)胞的機(jī)制,。就像特洛伊木馬一樣,，它們讓一種蛋白潛入宿主細(xì)胞來減弱宿主的免疫系統(tǒng)功能，從而為這種寄生菌侵入掃清道路,。這也是科學(xué)家第一次能夠證實宿主細(xì)胞表面蛋白上存在的化學(xué)修飾性氨基酸(sulpho-tyrosine,，即磺基酪氨酸)作為該寄生菌停靠和入侵的分子錨(molecular anchor),。
這一發(fā)現(xiàn)確實是一項影響深遠(yuǎn)的發(fā)現(xiàn),，因為這些磺基酪氨酸也在HIV病毒和瘧原蟲(plasmodium)---兩者分別是愛滋病(AIDS)和瘧疾的致病因子---感染它們的人類宿主過程當(dāng)中發(fā)揮著關(guān)鍵性作用。如今,，科學(xué)家相信他們已經(jīng)破解了不同寄生生物感染真核生物宿主時所采用的一種普遍適用的機(jī)制,。(生物谷：towersimper編譯)
doi:10.1073/pnas.1113775109
PMC:
PMID:
Host-targeting protein 1 (SpHtp1) from the oomycete Saprolegnia parasitica translocates specifically into fish cells in a tyrosine-O-sulphate–dependent manner
Stephan Wawra, Judith Bain, Elaine Durward, Irene de Bruijn, Kirsty L. Minor, Anja Matena, Lars Löbach, Stephen C. Whisson, Peter Bayer, Andrew J. Porter, Paul R. J. Birch, Chris J. Secombes, and Pieter van West
The eukaryotic oomycetes, or water molds, contain several species that are devastating pathogens of plants and animals. During infection, oomycetes translocate effector proteins into host cells, where they interfere with host-defense responses. For several oomycete effectors (i.e., the RxLR-effectors) it has been shown that their N-terminal polypeptides are important for the delivery into the host. Here we demonstrate that the putative RxLR-like effector, host-targeting protein 1 (SpHtp1), from the fish pathogen Saprolegnia parasitica translocates specifically inside host cells. We further demonstrate that cell-surface binding and uptake of this effector protein is mediated by an interaction with tyrosine-O-sulfate–modified cell-surface molecules and not via phospholipids, as has been reported for RxLR-effectors from plant pathogenic oomycetes. These results reveal an effector translocation route based on tyrosine-O-sulfate binding, which could be highly relevant for a wide range of host–microbe interactions.
