• 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 the CNGC20 Ca²⁺ ion channel is important for regulated immunity.

中文翻译：

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环核苷酸门控通道的调控不当介导了拟南芥中的胞质钙升高并激活了免疫

• 钙（Ca ²⁺）是植物细胞表面和细胞内受体的第二个信使，介导模式触发的免疫和效应器触发的免疫（分别为PTI和ETI）。几个环核苷酸门控通道（CNGC）已显示在PTI激活后控制瞬时的胞质Ca ^2+内流。目前尚不清楚CNGC特定成员对PTI和ETI的贡献。
• 增强性疾病易感性1（EDS1）调节ETI信号传导。在拟南芥基因屏幕的抑制器EDS1，我们确定在隐性增益的功能缺失突变CNGC20，表示cngc20-4，其中部分恢复抗病EDS1。
• cngc20-4增强PTI反应和ETI超敏细胞死亡。一个cngc20-4单个突变体表现出自身免疫性，这取决于遗传上平行的EDS1和水杨酸（SA）途径。CNGC20自缔合，与CNGC19形成异源复合物，并被BOTRYTIS诱导的KINASE1（BIK1）磷酸化并稳定。在预期的跨膜通道向内表面上的cngc20-4 L371F交换不会破坏这些相互作用，但会导致胞质Ca ²⁺积累增加，这与对CNGC20 Ca ²⁺渗透通道活性的错误调节一致。
• 我们的数据表明，由cngc20-4中的CNGC20突变形式引起的异位Ca ²⁺流入会影响PTI和ETI反应。我们得出的结论是，严格控制CNGC20 Ca ²⁺离子通道对于调节免疫力很重要。