The Ca ²⁺ Channel CYCLIC NUCLEOTIDE GATED CHANNEL13 (CNGC13) regulates systemic wound signalling and immunity against Spodoptera herbivory

Insect herbivory elicits rapid and complex signalling responses in plants, including membrane depolarization, cytosolic Ca ²⁺ elevation and activation of jasmonate-mediated defense pathways in local and systemic leaves. These early events are orchestrated by calcium-permeable channels and regulatory components that generate stimulus-specific cytosolic Ca ²⁺ signatures. However, the molecular mechanisms that generate long-distance Ca ²⁺ propagation and systemic immune activation on herbivory remain poorly defined. Here, we identify CYCLIC NUCLEOTIDE GATED CHANNEL13 (CNGC13) as a novel plasma membrane-localized, phloem-expressed Ca ²⁺ channel that is essential for systemic wound signalling and defense against lepidopteran pest, Spodoptera litura in Arabidopsis thaliana . CNGC13 is rapidly induced by wounding and herbivory, mediates cytosolic Ca ²⁺ influx, and is required for efficient propagation of Ca ²⁺ signals from wounded to distal leaves. Loss of CNGC13 compromises the thioglucosidase-dependent breakdown of aliphatic glucosinolates into aglucones/isothiocyanates within the vascular tissue, which are essential for wounding-induced systemic Ca ²⁺ wave propagation. Consequently, cngc13 mutants display impaired systemic jasmonate accumulation in distal leaves, reduced glucosinolate levels and enhanced herbivore susceptibility. CNGC13 is also required for At Pep-induced Ca ²⁺ elevation and Reactive Oxygen Species (ROS) signalling and interacts with the receptor kinase, PEPR2, implicating it in DAMP-mediated immune responses. Although CNGC13 and CNGC19 function cooperatively in herbivore defense, they do not physically interact, suggesting independent but converging roles. Our study identifies CNGC13 as a vasculature-localized Ca ²⁺ -permeable channel that functions downstream of PEPR2 receptor, to sustain systemic signalling, operating in a distinct yet converging pathway alongside known glutamate receptor-like channels during long-distance wound responses.