The Ca2+ channel CYCLIC NUCLEOTIDE GATED CHANNEL13 regulates vasculature-mediated systemic Ca2+ and jasmonate signaling on herbivory.

Insect herbivory triggers rapid local and systemic signaling in plants, including membrane depolarization, cytosolic Ca2+ 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 Ca2+ signatures. The glutamate receptor-like channel-centric model of long-distance Ca2+ signaling is insufficient to explain the robustness of systemic responses to diverse damage and herbivore cues, indicating the involvement of additional Ca2+ channels. Here, we identify CYCLIC NUCLEOTIDE GATED CHANNEL13 (CNGC13) as a plasma membrane-localized, vasculature-expressed Ca2+ 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 Ca2+ 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 Ca2+ 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 AtPep-induced Ca2+ 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 Ca2+-permeable channel that integrates multiple damage-cues, including Ricca factor and AtPep-PEPR signaling, to drive and sustain systemic signaling and immune activation.