Zhao Chunhui, Tang Yinhua, Wang Junli, Zeng Yanhong, Sun Hequan, Zheng Zichao, Su Rong, Schneeberger Korbinian, Parker Jane E, Cui Haitao
Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, Fujian University Key Laboratory for Plant-Microbe Interaction, Plant Immunity Center, Fujian Agriculture and Forestry University, Fuzhou, 350002, China.
Department of Plant-Microbe Interactions, Max-Planck Institute for Plant Breeding Research, Carl-von-Linné Weg 10, Cologne, 50829, Germany.
New Phytol. 2021 May;230(3):1078-1094. doi: 10.1111/nph.17218. Epub 2021 Feb 26.
Calcium (Ca ) is a second messenger for plant cell surface and intracellular receptors mediating pattern-triggered and effector-triggered immunity (respectively, PTI and ETI). Several CYCLIC NUCLEOTIDE-GATED CHANNELS (CNGCs) were shown to control transient cytosolic Ca influx upon PTI activation. The contributions of specific CNGC members to PTI and ETI remain unclear. ENHANCED DISEASE SUSCEPTIBLITY1 (EDS1) regulates ETI signaling. In an Arabidopsis genetic screen for suppressors of eds1, we identify a recessive gain-of-function mutation in CNGC20, denoted cngc20-4, which partially restores disease resistance in eds1. cngc20-4 enhances PTI responses and ETI hypersensitive cell death. A cngc20-4 single mutant exhibits autoimmunity, which is dependent on genetically parallel EDS1 and salicylic acid (SA) pathways. CNGC20 self-associates, forms heteromeric complexes with CNGC19, and is phosphorylated and stabilized by BOTRYTIS INDUCED KINASE1 (BIK1). The cngc20-4 L371F exchange on a predicted transmembrane channel inward surface does not disrupt these interactions but leads to increased cytosolic Ca accumulation, consistent with mis-regulation of CNGC20 Ca -permeable channel activity. Our data show that ectopic Ca influx caused by a mutant form of CNGC20 in cngc20-4 affects both PTI and ETI responses. We conclude that tight control of the CNGC20 Ca ion channel is important for regulated immunity.
钙（Ca²⁺）是植物细胞表面和细胞内受体的第二信使，分别介导模式触发免疫（PTI）和效应子触发免疫（ETI）。研究表明，几种环核苷酸门控通道（CNGCs）在PTI激活时控制细胞质中Ca²⁺的瞬时内流。特定CNGC成员对PTI和ETI的贡献仍不清楚。增强的疾病易感性1（EDS1）调节ETI信号传导。在对eds1抑制子的拟南芥遗传筛选中，我们鉴定出CNGC20中的一个隐性功能获得性突变，命名为cngc20-4，它部分恢复了eds1中的抗病性。cngc20-4增强了PTI反应和ETI超敏细胞死亡。cngc20-4单突变体表现出自发性免疫，这依赖于遗传上平行的EDS1和水杨酸（SA）途径。CNGC20自我缔合，与CNGC19形成异源复合物，并被葡萄孢诱导激酶1（BIK1）磷酸化和稳定。cngc20-4在预测的跨膜通道内向表面上的L371F交换不会破坏这些相互作用，但会导致细胞质中Ca²⁺积累增加，这与CNGC20 Ca²⁺通透通道活性的调节异常一致。我们的数据表明，cngc20-4中CNGC20突变形式引起的异位Ca²⁺内流影响PTI和ETI反应。我们得出结论，对CNGC20 Ca²⁺离子通道的严格控制对调节免疫很重要。
