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并抑制番茄中由青枯雷尔氏菌诱导的过敏反应和非寄主抗性。

and Suppress pv. -Induced Hypersensitive Response and Non-host Resistance in Tomato.

作者信息

Zhang Xuan-Rui, Xu You-Ping, Cai Xin-Zhong

机构信息

Institute of Biotechnology, College of Agriculture and Biotechnology, Zhejiang University, Hangzhou, China.

Center of Analysis and Measurement, Zhejiang University, Hangzhou, China.

出版信息

Front Plant Sci. 2018 Mar 6;9:285. doi: 10.3389/fpls.2018.00285. eCollection 2018.

DOI:10.3389/fpls.2018.00285
PMID:29559989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5845538/
Abstract

Mechanisms underlying plant non-host resistance to pv. (), the pathogen causing rice leaf streak disease, are largely unknown. Cyclic nucleotide-gated ion channels (CNGCs) are calcium-permeable channels that are involved in various biological processes including plant resistance. In this study, functions of two tomato genes and in non-host resistance to were analyzed. Silencing of and in tomato significantly enhanced -induced hypersensitive response (HR) and non-host resistance, demonstrating that both and negatively regulate non-host resistance related HR and non-host resistance to in tomato. Silencing of and strikingly increased -induced callose deposition and strongly promoted both -induced and flg22-elicited HO, indicating that these two repress callose deposition and ROS accumulation to attenuate non-host resistance and PAMP-triggered immunity (PTI). Importantly, silencing of and apparently compromised cytosolic Ca accumulation, implying that SlCNGC1 and SlCNGC14 function as Ca channels and negatively regulate non-host resistance and PTI-related responses through modulating cytosolic Ca accumulation. seemed to play a stronger regulatory role in the non-host resistance and PTI compared to . Our results reveal the contribution of CNGCs and probably also Ca signaling pathway to non-host resistance and PTI.

摘要

引起水稻条斑病的病原菌(水稻条斑病菌),其在植物非寄主抗性中的潜在机制很大程度上尚不清楚。环核苷酸门控离子通道(CNGCs)是钙通透性通道,参与包括植物抗性在内的各种生物学过程。在本研究中,分析了番茄中两个基因SlCNGC1和SlCNGC14在对水稻条斑病菌的非寄主抗性中的功能。番茄中SlCNGC1和SlCNGC14的沉默显著增强了水稻条斑病菌诱导的过敏反应(HR)和非寄主抗性,表明SlCNGC1和SlCNGC14均负向调节番茄中与非寄主抗性相关的HR和对水稻条斑病菌的非寄主抗性。SlCNGC1和SlCNGC14的沉默显著增加了水稻条斑病菌诱导的胼胝质沉积,并强烈促进了水稻条斑病菌诱导的和flg22诱导的活性氧(ROS)产生,表明这两个基因抑制胼胝质沉积和ROS积累以减弱非寄主抗性和病原体相关分子模式触发的免疫(PTI)。重要的是,SlCNGC1和SlCNGC14的沉默明显损害了胞质钙积累,这意味着SlCNGC1和SlCNGC14作为钙通道发挥作用,并通过调节胞质钙积累负向调节非寄主抗性和PTI相关反应。与SlCNGC14相比,SlCNGC1似乎在非寄主抗性和PTI中发挥更强的调节作用。我们的结果揭示了CNGCs以及可能还有钙信号通路对非寄主抗性和PTI的贡献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/cd3088d08c52/fpls-09-00285-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/4da27767c625/fpls-09-00285-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/c38081621372/fpls-09-00285-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/115051913247/fpls-09-00285-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/d94cb12d65bb/fpls-09-00285-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/cd3088d08c52/fpls-09-00285-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/4da27767c625/fpls-09-00285-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/c38081621372/fpls-09-00285-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/115051913247/fpls-09-00285-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/d94cb12d65bb/fpls-09-00285-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e14d/5845538/cd3088d08c52/fpls-09-00285-g005.jpg

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