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首页> 外文期刊>Current Biology: CB >FERONIA Receptor Kinase Contributes to Plant Immunity by Suppressing Jasmonic Acid Signaling in ce:italic>Arabidopsis thaliana/ce:italic>
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FERONIA Receptor Kinase Contributes to Plant Immunity by Suppressing Jasmonic Acid Signaling in ce:italic>Arabidopsis thaliana/ce:italic>

机译：Feronia受体激酶通过抑制茉莉酸信号传导在＆ Ce：斜视> rapidopsis thaliana＆ / ce：斜体>

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摘要

Bacterial pathogens use effectors and phytotoxins to facilitate infection of host plants. Coronatine (COR) is one of the phytotoxins produced in bacterial pathogens, such asPseudomonas syringaepv. tomato DC3000 (pst DC3000). COR structurally and functionally mimics the active form of the plant hormone jasmonic acid (JA), JA-isoleucine (JA-Ile), and can hijack the host JA-signaling pathway to achieve host disease susceptibility []. COR utilizes the transcription factor MYC2, a master regulator of JA signaling, to activate NAC transcription factors, which functions to inhibit accumulation of salicylic acid (SA) and thus compromise host immunity []. It?has been demonstrated that SA can antagonize?JA?signaling through NONEXPRESSOR of PATHOGENESIS-RELATED GENE1 (NPR1) [] and downstream transcription factors TGAs [] and WRKYs []. However, the detailed mechanism by which host plants counteract COR-mediated susceptibility is largely unknown. Here, we show that the receptor kinase FERONIA (FER) functions to inhibit JA and COR signaling by phosphorylating and destabilizing MYC2, thereby positively regulating immunity. Conversely, the peptide ligand RALF23 acts through FER to stabilize MYC2 and elevate JA signaling, negatively contributing to plant immunity. Our results establish the RALF23-FER-MYC2 signaling module and provide a previously unknown mechanism by which host plants utilize FER signaling to counteract COR-mediated host disease susceptibility.
机译：细菌病原体使用效果和植物毒素，以促进宿主植物的感染。冠状胺（Cor）是细菌病原体中产生的植物毒素之一，这种aspseudomonas syringaepv。番茄DC3000（PST DC3000）。在结构上和功能上模仿植物激素茉莉酸（JA），JA-异亮氨酸（JA-ILE）的活性形式，可以劫持宿主JA信号通路以实现宿主疾病易感性[]。 Cor利用转录因子MyC2，JA信号传导的主调节器，激活NAC转录因子，其用于抑制水杨酸（SA）的积累，从而损害宿主免疫[]。它已被证明SA可以拮抗α~~通过致病性相关的基因1（NPR1）[]和下游转录因子TGA []和WRKYS []信号传导。然而，宿主植物抵消了COR介导的易感性的详细机制在很大程度上是未知的。在这里，我们表明受体激酶feronia（FER）通过磷酸化和稳定的Myc2来抑制Ja和Cor信号传导，从而正常调节免疫力。相反，肽配体RALF23通过FER稳定MyC2并提高JA信号，对植物免疫产生负面影响。我们的结果建立了RALF23-FER-MYC2信令模块，并提供了先前未知的机制，宿主工厂利用FER信号来抵消COR介导的宿主疾病易感性。

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