生物谷Bioon.com 訊 據(jù)NIBS網(wǎng)站最新報(bào)道,，2010年8月1日,，北京生命科學(xué)研究所張躍林領(lǐng)導(dǎo)的研究組篩選出了一重要突變體snc4-1D。該研究成果發(fā)表于國際知名學(xué)術(shù)雜志《植物生理學(xué)》（Plant Physiology）上,。
植物在與病原菌長期的共同演化過程中,，針對(duì)病原菌的多種致病因素，發(fā)展了極其復(fù)雜的抗病機(jī)制,。PAMPs（Pathogen-Associate Molecular Patterns）激發(fā)的免疫反應(yīng)是其中一類重要的抗病機(jī)制,。
PRRs中最重要的一類受體是RLKs（Receptor-like kinases）。為了進(jìn)一步尋找抗病途徑中的新組分,，我們篩選找到一個(gè)重要的突變體：snc4-1D,。snc4-1D是在Col-0背景下通過EMS誘變用于篩選抗病反應(yīng)途徑中的新組分得到的，它是一個(gè)半顯性且具有與snc1類似表型特征的突變體,。SNC4的圖位克隆表明它是一個(gè)非典型的受體類蛋白激酶,，該激酶具有兩個(gè)細(xì)胞外的GDPD結(jié)構(gòu)。snc4-1D在細(xì)胞內(nèi)的激酶區(qū)發(fā)生了一個(gè)從丙氨酸到蘇氨酸的點(diǎn)突變,。通過用snc4-1D轉(zhuǎn)化野生型植物,，得到的轉(zhuǎn)基因植物同snc4-1D的突變體的表型一致，這表明該突變體是一個(gè)功能獲得性的突變體,。實(shí)驗(yàn)結(jié)果表明ndr1而不是eds1可以抑制該突變體植物的表型,。除此之外，MKS的T-DNA插入突變體（同MPK4相關(guān)的一個(gè)正向調(diào)控蛋白）也可以部分抑制snc4-1D的表型,。而且該突變體的外部形態(tài)和持續(xù)對(duì)病原菌的抵抗也可以部分被茉莉酸（JA）所抑制,，由此表明JA在snc4-1D介導(dǎo)的抗病反應(yīng)中發(fā)揮了作用。snc4-1D的發(fā)現(xiàn)為我們提供了一個(gè)有效的遺傳工具,，從而用于分析受體類蛋白激酶下游的信號(hào)傳導(dǎo)機(jī)制,。
畢冬玲為該論文的第一作者，其他作者還有加拿大UBC大學(xué)的博士研究生Cheng YuTi和李昕教授,，北京生命科學(xué)研究所的張躍林博士為本論文的通訊作者,。此項(xiàng)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：
Plant Physiology 153:1771-1779 (2010) DOI:10.1104/pp.110.15850
Activation of Plant Immune Responses by a Gain-of-Function Mutation in an Atypical Receptor-Like Kinase1,[C],[W],[OA]
Dongling Bi, Yu Ti Cheng, Xin Li and Yuelin Zhang*
State Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, China Agricultural University, Beijing 100094, People's Republic of China (D.B.); National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 102206, People's Republic of China (D.B., Y.Z.); Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z4 (Y.T.C., X.L.)
Arabidopsis (Arabidopsis thaliana) suppressor of npr1-1, constitutive1 (snc1) contains a gain-of-function mutation in a Toll/interleukin receptor-nucleotide binding site-leucine-rich repeat Resistance (R) protein and it has been a useful tool for dissecting R-protein-mediated immunity. Here we report the identification and characterization of snc4-1D, a semidominant mutant with snc1-like phenotypes. snc4-1D constitutively expresses defense marker genes PR1, PR2, and PDF1.2, and displays enhanced pathogen resistance. Map-based cloning of SNC4 revealed that it encodes an atypical receptor-like kinase with two predicted extracellular glycerophosphoryl diester phosphodiesterase domains. The snc4-1D mutation changes an alanine to threonine in the predicted cytoplasmic kinase domain. Wild-type plants transformed with the mutant snc4-1D gene displayed similar phenotypes as snc4-1D, suggesting that the mutation is a gain-of-function mutation. Epistasis analysis showed that NON-RACE-SPECIFIC DISEASE RESISTANCE1 is required for the snc4-1D mutant phenotypes. In addition, the snc4-1D mutant phenotypes are partially suppressed by knocking out MAP KINASE SUBSTRATE1, a positive defense regulator associated with MAP KINASE4. Furthermore, both the morphology and constitutive pathogen resistance of snc4-1D are partially suppressed by blocking jasmonic acid synthesis, suggesting that jasmonic acid plays an important role in snc4-1D-mediated resistance. Identification of snc4-1D provides us a unique genetic system for analyzing the signal transduction pathways downstream of receptor-like kinases.
