Abstract

Soil salinity severely threatens plant growth and crop production. Although the cytosolic Ca 2+ elevation in response to osmotic stress plays essential roles in plant salt response, the mechanisms underlying Ca 2+ signal generation upon salt stress remain largely unknown. Here, we report that the cyclic nucleotide-gated channel 7 (OsCNGC7), together with Ca 2+ -dependent protein kinase 4 (OsCPK4), forms a module to fine-tune salt stress responses in rice. OsCNGC7 positively regulates rice salt tolerance by elevating cytosolic Ca 2+ levels, and its loss-of-function mutants exhibit salt-sensitive phenotypes and impaired salt-triggered Ca 2+ influx. Mechanistic investigations revealed that early salt stress increases the kinase activity of OsCPK4, which phosphorylates OsCNGC7 to enhance its channel activity and protein stability for rapid Ca 2+ influx, thus rapidly triggering downstream responses to cope with salt stress. During prolonged salt stress, the kinase activity of OsCPK4 is suppressed, which results in decreased phosphorylation as well as protein abundance of OsCNGC7, thereby reducing Ca 2+ -mediated salt stress response. Therefore, OsCPK4-mediated phosphorylation fine-tunes the channel activity and protein stability of OsCNGC7, which ensures triggering rapid salt stress response followed by growth recovery. Our findings reveal a novel molecular module OsCPK4-OsCNGC7, which provides an auto-regulatory mechanism for salt stress adaptation in rice through fine-tuning Ca 2+ influx, achieving the balance between plant growth and stress responses.