The Ca 2+ channel CYCLIC NUCLEOTIDE GATED CHANNEL13 regulates vasculature-mediated systemic Ca 2+ and jasmonate signaling on herbivory

Insect herbivory triggers rapid local and systemic signaling in plants, including membrane depolarization, cytosolic Ca 2+ elevation, and activation of jasmonate-mediated defense pathways. These early events are shaped by calcium-permeable ion channels and regulatory components that generate stimulus-specific Ca 2+ signatures. The glutamate receptor-like channel-centric model of long-distance Ca 2+ signaling is insufficient to explain the robustness of systemic responses to diverse damage and herbivore cues, indicating the involvement of additional Ca 2+ channels. Here, we identify CYCLIC NUCLEOTIDE GATED CHANNEL13 (CNGC13) as a plasma membrane–localized, vasculature-expressed Ca 2+ channel that is essential for systemic jasmonate signaling and defense against lepidopteran insect pest, Spodoptera litura in Arabidopsis thaliana . CNGC13 is rapidly induced by wounding and herbivory and is required for efficient propagation of Ca 2+ signals from wounded to distal leaves. Loss of CNGC13 compromises the thioglucosidase (Ricca factor)-dependent breakdown of aliphatic glucosinolates into aglucones/isothiocyanates within the vascular tissue, which are essential for wound-induced systemic Ca 2+ wave propagation. Consequently, cngc13 mutants display reduced wound induced jasmonate accumulation in systemic leaves, reduced glucosinolate levels and enhanced herbivore susceptibility. CNGC13 is also required for At Pep-induced Ca 2+ elevation and reactive oxygen species signaling and physically interacts with PLANT ELICITOR PEPTIDE RECEPTOR 2 (PEPR2) kinase domain. Consistently, pepr2 mutants display similar defects in glucosinolate aglucone production and systemic jasmonate accumulation. Together, our findings identify CNGC13 as a vasculature-localized Ca 2+ -permeable channel that integrates multiple damage-cues, including Ricca factor and At Pep-PEPR signaling, to drive and sustain systemic signaling and immune activation.