近日來自北京生命科學(xué)研究所的研究人員在《公共科學(xué)圖書館—遺傳學(xué)》(PLoS Genetics)雜志上發(fā)表題為“Transportin-SR Is Required for Proper Splicing of Resistance Genes and Plant Immunity”的文章。
這篇文章的通訊作者是北京生命科學(xué)研究所的青年研究員張躍林博士,,其早年畢業(yè)于復(fù)旦大學(xué)遺傳學(xué)及遺傳工程專業(yè),,實驗室的研究方向主要為先天性免疫和功能基因組學(xué)。博士研究生許少華為本文的第一作者,,參與此工作的還有張志斌,、荊貝貝和丁金美以及University of British Columbia的Patrick Gannon、徐芳和李昕教授,。
由植物抗性 (Resistance, R) 基因編碼的免疫受體在植物抗擊病原菌的免疫過程中發(fā)揮了重要作用,。植物中很多R基因,包括SNC1和RPS4都存在選擇性剪接,,然而植物體調(diào)控R基因剪接的機制目前還知之甚少,。
在這篇文章中,研究人員證實MOS14 (modifier of snc1-1, 14)的突變抑制了snc1植物中組成性激活的免疫反應(yīng),。圖位克隆和生物信息學(xué)分析顯示MOS14編碼了一個和動物中Transportin-SR (TRN-SR) 存在序列相似性的蛋白,。TRN-SR是importin-beta超家族的一個成員,,它負(fù)責(zé)serine-arginine rich (SR) 蛋白的入核轉(zhuǎn)運,而SR蛋白在RNA代謝過程中發(fā)揮著重要作用,。熒光共聚焦實驗顯示MOS14定位在細(xì)胞核中,,酵母雙雜交顯示MOS14的C端可以和SR蛋白相互作用,其N端可以和小G蛋白AtRAN1相互作用,。SR蛋白在Col-0中定位于細(xì)胞核,,然而在mos14-1突變體中,SR蛋白卻分散在整個細(xì)胞中,。另外,,有幾個發(fā)生選擇性剪接的基因在mos14-1中的選擇性剪接模式發(fā)生了改變,這些實驗證明MOS14編碼了擬南芥中一個TRN-SR蛋白,。
進(jìn)一步實驗表明MOS14的突變導(dǎo)致了SNC1和RPS4這兩個R基因選擇性剪接模式的改變,,從而減弱了它們激活的免疫反應(yīng)。這些實驗結(jié)果顯示,,由MOS14介導(dǎo)的SR蛋白的入核對于這兩個R基因的正確剪接以及它們在植物中介導(dǎo)的免疫反應(yīng)是非常重要的,。
此項研究為科技部和北京市科委資助課題,在北京生命科學(xué)研究所完成,。(生物谷Bioon.com)
生物谷推薦原文出處:
PLoS Genetics doi:10.1371/journal.pgen.1002159.g001
Transportin-SR Is Required for Proper Splicing of Resistance Genes and Plant Immunity
Shaohua Xu, Zhibin Zhang, Beibei Jing, Patrick Gannon, Jinmei Ding, Fang Xu, Xin Li, Yuelin Zhang
Transportin-SR (TRN-SR) is a member of the importin-β super-family that functions as the nuclear import receptor for serine-arginine rich (SR) proteins, which play diverse roles in RNA metabolism. Here we report the identification and cloning of mos14 (modifier of snc1-1, 14), a mutation that suppresses the immune responses conditioned by the auto-activated Resistance (R) protein snc1 (suppressor of npr1-1, constitutive 1). MOS14 encodes a nuclear protein with high similarity to previously characterized TRN-SR proteins in animals. Yeast two-hybrid assays showed that MOS14 interacts with AtRAN1 via its N-terminus and SR proteins via its C-terminus. In mos14-1, localization of several SR proteins to the nucleus was impaired, confirming that MOS14 functions as a TRN-SR. The mos14-1 mutation results in altered splicing patterns of SNC1 and another R gene RPS4 and compromised resistance mediated by snc1 and RPS4, suggesting that nuclear import of SR proteins by MOS14 is required for proper splicing of these two R genes and is important for their functions in plant immunity.