张跃林博士早年毕业于复旦大学遗传学及遗传工程专业，实验室的研究方向主要为先天性免疫和功能基因组学。近期其研究小组发表文章，解析植物功能基因组研究。
研究人员们筛选找到一个重要的突变体：snc4-1D，这为进一步寻找抗病途径中的新组分提供了重要的信息，这一研究成果公布在《植物生理学》（Plant Physiology）杂志上。
植物在与病原菌长期的共同演化过程中，针对病原菌的多种致病因素，发展了极其复杂的抗病机制。PAMPs（Pathogen-Associate Molecular Patterns）激发的免疫反应是其中一类重要的抗病机制。PRRs中最重要的一类受体是RLKs（Receptor-like kinases）。
为了进一步寻找抗病途径中的新组分，我们筛选找到一个重要的突变体：snc4-1D。snc4-1D是在Col-0背景下通过EMS诱变用于筛选抗病反应途径中的新组分得到的，它是一个半显性且具有与snc1类似表型特征的突变体。SNC4的图位克隆表明它是一个非典型的受体类蛋白激酶，该激酶具有两个细胞外的GDPD结构。snc4-1D在细胞内的激酶区发生了一个从丙氨酸到苏氨酸的点突变。通过用snc4-1D转化野生型植物，得到的转基因植物同snc4-1D的突变体的表型一致，这表明该突变体是一个功能获得性的突变体。实验结果表明ndr1而不是eds1可以抑制该突变体植物的表型。除此之外，MKS的T-DNA插入突变体（同MPK4相关的一个正向调控蛋白）也可以部分抑制snc4-1D的表型。而且该突变体的外部形态和持续对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介导的抗病反应中发挥了作用。snc4-1D的发现为我们提供了一个有效的遗传工具，从而用于分析受体类蛋白激酶下游的信号传导机制。
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《植物生理学》发表论文摘要（英文）
全文下载：https://www.plantphysiol.org/cgi/reprint/153/4/1771.pdf
First published online May 27, 2010; 10.1104/pp.110.158501
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.
