The OsCPK4-OsCNGC7 phosphorylation-centered feedback loop promotes Ca²⁺ influx and confers salt tolerance in rice

Soil salinity severely threatens plant growth and crop production. Although elevated cytosolic Ca²⁺ levels in response to osmotic stress are essential for plant responses to salt stress, the mechanisms underlying the generation and regulation of these Ca²⁺ signals remain largely unknown. Here, we report that rice cyclic nucleotide-gated channel 7 (OsCNGC7) forms a regulatory module with Ca²⁺-dependent protein kinase 4 (OsCPK4) to fine-tune salt-stress responses. OsCNGC7 promotes salt tolerance by mediating Ca²⁺ influx, whereas loss of OsCNGC7function increases salt sensitivity and impairs salt-induced Ca²⁺ influx. Mechanistic analyses revealed that, during the early phase of salt stress, enhanced OsCPK4 kinase activity promotes the phosphorylation of OsCNGC7, thereby increasing its channel activity and protein stability. The resulting Ca²⁺ influx rapidly activates downstream salt-stress responses. During prolonged salt stress, OsCPK4 kinase activity is suppressed, reducing the phosphorylation and protein abundance of OsCNGC7 and thereby inhibiting Ca²⁺-mediated salt-stress responses. OsCPK4-mediated phosphorylation thus fine-tunes OsCNGC7 channel activity and stability, enabling the rapid activation of salt-stress responses followed by their timely attenuation to facilitate growth recovery. Our findings reveal that the OsCPK4-OsCNGC7 module provides an auto-regulatory mechanism for salt-stress adaptation in rice that dynamically modulates Ca²⁺ influx to balance stress tolerance with growth.