Nucleoporin-Regulated MAP Kinase Signaling in Immunity to a Necrotrophic Fungal Pathogen
Nucleoporin-Regulated MAP Kinase Signaling in Immunity to a Necrotrophic Fungal Pathogen
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DOI：
10.1104/pp.16.00832
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发表时间：
2016-10-01
期刊：
影响因子：
7.4
通讯作者：
Wiermer, Marcel
中科院分区：
文献类型：
--
作者：
Genenncher, Bianca;Wirthmueller, Lennart;Wiermer, Marcel
病原体应答性丝裂原活化蛋白激酶（MAPK或MPK）级联将信号从活化的免疫受体穿过核膜传递到核内靶点。然而，在植物中，对MAPK信号的空间控制知之甚少。在这里，我们报告说，拟南芥（拟南芥）核孔复合体蛋白Nup 88/MOS 7是必不可少的免疫坏死营养型真菌灰葡萄孢。mos 7 -1突变导致4个氨基酸缺失，危及B。灰衣诱导的关键免疫调节MAPK MPK 3/MPK 6的激活，并降低MPK 3蛋白水平转录后。此外，MOS 7有助于在细胞核中保留足够的MPK 3丰度，这是对B的完全免疫所需的。灰叶最后，我们提出了MOS 7的结构模型，并表明mos 7 -1突变妥协与Nup 98 a/B，两个苯丙氨酸-甘氨酸重复核孔蛋白的相互作用，涉及维持选择性核孔复合物的渗透性屏障。总之，我们的分析揭示了MOS 7和Nup 98作为植物对坏死性病原体免疫的新组分，并提供了这些核孔蛋白如何协调核质运输以产生强大的免疫反应的机制见解。
Pathogen-responsive mitogen-activated protein kinase (MAPK or MPK) cascades relay signals from activated immune receptors across the nuclear envelope to intranuclear targets. However, in plants, little is known about the spatial control of MAPK signaling. Here, we report that the Arabidopsis (Arabidopsis thaliana) nuclear pore complex protein Nup88/MOS7 is essential for immunity to the necrotrophic fungus Botrytis cinerea. The mos7-1 mutation, causing a four-amino acid deletion, compromises B. cinerea-induced activation of the key immunoregulatory MAPKs MPK3/MPK6 and reduces MPK3 protein levels posttranscriptionally. Furthermore, MOS7 contributes to retaining a sufficient MPK3 abundance in the nucleus, which is required for full immunity to B. cinerea. Finally, we present a structural model of MOS7 and show that the mos7-1 mutation compromises interactions with Nup98a/b, two phenylalanine-glycine repeat nucleoporins implicated in maintaining the selective nuclear pore complex permeability barrier. Together, our analysis uncovered MOS7 and Nup98 as novel components of plant immunity toward a necrotrophic pathogen and provides mechanistic insights into how these nucleoporins coordinate nucleocytoplasmic transport to mount a robust immune response.