A mis-regulated cyclic nucleotide-gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis
A mis-regulated cyclic nucleotide-gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis
复制标题
拟南芥中错误调节的环核苷酸门控通道介导细胞质钙升高并激活免疫力。
DOI：
10.1111/nph.17218
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发表时间：
2021-02-26
期刊：
影响因子：
9.4
通讯作者：
Cui, Haitao
中科院分区：
文献类型：
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作者：
Zhao, Chunhui;Tang, Yinhua;Cui, Haitao
钙（Ca 2+）是植物细胞表面和细胞内受体的第二信使，介导模式触发和效应物触发的免疫（分别为PTI和ETI）。几个环核苷酸门控通道（CNGC）被证明可以控制PTI激活后瞬时胞质Ca 2+内流。具体CNGC成员对PTI和ETI的贡献尚不清楚。增强的疾病易感性1（EDS 1）调节ETI信号传导。在拟南芥的eds 1抑制基因筛选中，我们发现了CNGC 20中的一个隐性功能获得性突变，表示为cngc 20 -4，它部分恢复了eds 1的抗病性。cngc 20 -4增强PTI应答和ETI过敏性细胞死亡。cngc 20 -4单突变体表现出自身免疫性，其依赖于遗传上平行的EDS 1和水杨酸（SA）途径。CNGC 20自我缔合，与CNGC 19形成异聚体复合物，并被葡萄球菌诱导的激酶1（BIK 1）磷酸化和稳定化。预测的跨膜通道向内表面上的cngc 20 -4 L371 F交换不会破坏这些相互作用，但会导致胞质Ca 2+积累增加，这与CNGC 20 Ca 2+渗透通道活性的误调节一致。我们的数据表明，cngc 20 -4中CNGC 20的突变形式引起的异位Ca 2+内流影响PTI和ETI反应。我们的结论是，CNGC 20钙离子通道的严格控制是重要的调节免疫。
Calcium (Ca2+ ) 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 Ca2+ 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 Ca2+ accumulation, consistent with mis-regulation of CNGC20 Ca2+ -permeable channel activity. Our data show that ectopic Ca2+ influx caused by a mutant form of CNGC20 in cngc20-4 affects both PTI and ETI responses. We conclude that tight control of CNGC20 Ca2+ ion channel is important for regulated immunity.