Antagonism of Transcription Factor MYC2 by EDS1/PAD4 Complexes Bolsters Salicylic Acid Defense in Arabidopsis Effector-Triggered Immunity
Antagonism of Transcription Factor MYC2 by EDS1/PAD4 Complexes Bolsters Salicylic Acid Defense in Arabidopsis Effector-Triggered Immunity
复制标题
EDS1/PAD4 复合物对转录因子 MYC2 的拮抗作用增强拟南芥效应子触发免疫中的水杨酸防御
DOI：
10.1016/j.molp.2018.05.007
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发表时间：
2018-08-06
期刊：
影响因子：
27.5
通讯作者：
Parker, Jane E.
中科院分区：
文献类型：
--
作者：
Cui, Haitao;Qiu, Jingde;Parker, Jane E.
在植物免疫中，病原体激活的细胞内核苷酸结合/富含亮氨酸重复序列（NLR）受体调动抗病途径，但下游信号传导机制仍不清楚。增强疾病易感性 1 (EDS1) 控制由 Toll-白细胞介素 1 受体结构域 (TIR) 家族 NLR (TNL) 触发的抗性转录重编程。水杨酸 (SA) 激素防御区的转录诱导是对抗生物营养病原体的重要屏障。在这里，我们提出了遗传和分子证据，表明在拟南芥中，EDS1 复合物与其伴侣 PAD4 抑制 MYC2，MYC2 是 SA 拮抗茉莉酸 (JA) 激素途径的主要调节因子。在 TNL 免疫反应中，EDS1/PAD4 对 MYC2 的干扰可独立于 EDS1 诱导的 SA 合成来增强 SA 防御区，从而有效阻断有效的细菌 JA 模拟物冠菌素 (COR) 的作用。我们表明，MYC2 的拮抗作用发生在细胞核内检测到 COR 之后，但在 MYC2 与靶启动子 pANAC019 结合之前或同时发生。 PAD4 与 MYC2 在植物中的稳定相互作用由 EDS1-PAD4 复合物竞争。然而，抑制 MYC2 启动基因需要 EDS1 和 PAD4，这表明 EDS1-PAD4 异二聚体活性在 MYC2 抑制中至关重要。总而言之，这些结果揭示了一个免疫受体信号传导回路，该信号传导回路与激素途径串扰相交叉，以减少细菌病原体的生长。
In plant immunity, pathogen-activated intracellular nucleotide binding/leucine rich repeat (NLR) receptors mobilize disease resistance pathways, but the downstream signaling mechanisms remain obscure. Enhanced disease susceptibility 1 (EDS1) controls transcriptional reprogramming in resistance triggered by Toll-Interleukin1-Receptor domain (TIR)-family NLRs (TNLs). Transcriptional induction of the salicylic acid (SA) hormone defense sector provides one crucial barrier against biotrophic pathogens. Here, we present genetic and molecular evidence that in Arabidopsis an EDS1 complex with its partner PAD4 inhibits MYC2, a master regulator of SA-antagonizing jasmonic acid (JA) hormone pathways. In the TNL immune response, EDS1/PAD4 interference with MYC2 boosts the SA defense sector independently of EDS1-induced SA synthesis, thereby effectively blocking actions of a potent bacterial JA mimic, coronatine (COR). We show that antagonism of MYC2 occurs after COR has been sensed inside the nucleus but before or coincident with MYC2 binding to a target promoter, pANAC019. The stable interaction of PAD4 with MYC2 in planta is competed by EDS1-PAD4 complexes. However, suppression of MYC2-promoted genes requires EDS1 together with PAD4, pointing to an essential EDS1-PAD4 heterodimer activity in MYC2 inhibition. Taken together, these results uncover an immune receptor signaling circuit that intersects with hormone pathway crosstalk to reduce bacterial pathogen growth.