突变体snc4-1D发现 植物抗病机制新进展

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突变体snc4-1D发现 植物抗病机制新进展

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PNAS：突变体snc四-一D发现 植物抗病机制新进展据NIBS网站最新报道，二零一零年八月一日，北京生命科学研究所张跃林领导的研究组筛选出了1重要突变体snc四-一D。该研究成果发表于国际知名学术杂志｛植物生理学｝（Plant Physiology）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1类重要的抗病机制。

PRRs中最重要的1类受体是RLKs（Receptor-like kinases）。为了进1步寻找抗病途径中的新组分，我们筛选找到1个重要的突变体：snc四-一D。snc四-一D是在Col-零配景下通过EMS诱变用于筛选抗病反应途径中的新组分得到的，它是1个半显性且具有与snc一类似表型特征的突变体。SNC四的图位克隆表白它是1个非典型的受体类蛋利剑激酶，该激酶具有两个细胞外的GDPD结构。snc四-一D在细胞内的激酶区发生了1个从丙氨酸到苏氨酸的点突变。通过用snc四-一D转化野生型植物，得到的转基因植物同snc四-一D的突变体的表型1致，这表白该突变体是1个功能获得性的突变体。实验结果表白ndr一而不是eds一可以按捺该突变体植物的表型。除此之外，MKS的T-DNA插入突变体（同MPK四相关的1个正向调控蛋利剑）也可以部分按捺snc四-一D的表型。并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）所按捺，由此表白JA在snc四-一D介导的抗病反应中发挥了作用。snc四-一D的发现为我们提供了1个有效的遗传工具，从而用于分析受体类蛋利剑激酶下游的信号传导机制。

毕冬玲为该论文的第1作者，其他作者还有加拿大UBC大学的博士研究生Cheng YuTi和李昕教授，北京生命科学研究所的张跃林博士为本论文的通讯作者。此项研究为科技部和北京市科委帮助课题，在北京生命科学研究所完成。（生物谷

生物谷保举原文出处：

Plant Physiology 一五三:一七七一-一七七九 (二零一零) DOI:一零.一一零四/pp.一一零.一五八五零

Activation of Plant Immune Responses by a Gain-of-Function Mutation in an Atypical Receptor-Like Kinase一,[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 一零零零九四, People‘s Republic of China (D.B.); National Institute of Biological Sciences, Zhongguancun Life Science Park, Beijing 一零二二零六, People‘s Republic of China (D.B., Y.Z.); Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, Canada V六T 一Z四 (Y.T.C., X.L.)

Arabidopsis (Arabidopsis thaliana) suppressor of npr一-一, constitutive一 (snc一) 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 snc四-一D, a semidominant mutant with snc一-like phenotypes. snc四-一D constitutively expresses defense marker genes PR一, PR二, and PDF一.二, and displays enhanced pathogen resistance. Map-based cloning of SNC四 revealed that it encodes an atypical receptor-like kinase with two predicted extracellular glycerophosphoryl diester phosphodiesterase domains. The snc四-一D mutation changes an alanine to threonine in the predicted cytoplasmic kinase domain. Wild-type plants transformed with the mutant snc四-一D gene displayed similar phenotypes as snc四-一D, suggesting that the mutation is a gain-of-function mutation. Epistasis analysis showed that NON-RACE-SPECIFIC DISEASE RESISTANCE一 is required for the snc四-一D mutant phenotypes. In addition, the snc四-一D mutant phenotypes are partially suppressed by knocking out MAP KINASE SUBSTRATE一, a positive defense regulator associated with MAP KINASE四. Furthermore, both the morphology and constitutive pathogen resistance of snc四-一D are partially suppressed by blocking jasmonic acid synthesis, suggesting that jasmonic acid plays an important role in snc四-一D-mediated resistance. Identification of snc四-一D provides us a unique genetic system for analyzing the signal transduction pathways downstream of receptor-like kinases.

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