A mis?regulated cyclic nucleotide?gated channel mediates cytosolic calcium elevation and activates immunity in Arabidopsis

Calcium (Ca2+) is a second messenger for plant cell surface and intracellular receptors mediating pattern-triggered effector-triggered immunity (respectively, PTI ETI). Several CYCLIC NUCLEOTIDE-GATED CHANNELS (CNGCs) were shown to control transient cytosolic Ca2+ influx upon activation. The contributions of specific CNGC members ETI remain unclear. ENHANCED DISEASE SUSCEPTIBLITY1 (EDS1) regulates signaling. In an Arabidopsis genetic screen suppressors eds1, we identify recessive gain-of-function mutation in CNGC20, denoted cngc20-4, which partially restores disease resistance eds1. cngc20-4 enhances responses hypersensitive death. A single mutant exhibits autoimmunity, dependent on genetically parallel EDS1 salicylic acid (SA) pathways. CNGC20 self-associates, forms heteromeric complexes with CNGC19, phosphorylated stabilized by BOTRYTIS INDUCED KINASE1 (BIK1). L371F exchange predicted transmembrane channel inward does not disrupt these interactions but leads increased accumulation, consistent mis-regulation Ca2+-permeable activity. Our data show that ectopic caused form affects both responses. We conclude tight the ion important regulated immunity.