LAUSR

Nitrate-induced Ca2+ signaling is crucial for the primary nitrate response in plants. However, the molecular mechanism for generating nitrate-specific calcium signature remains unknown. We report here that a cyclic nucleotide-gated channel (CNGC) protein, CNGC15, and the nitrate transceptor (NRT1.1) constitute a molecular switch that controls calcium influx depending on nitrate levels. CNGC15 gene expression was induced by nitrate and the CNGC15 protein was localized to the plasma membrane after establishment of young seedlings. Disruption of CNGC15 gene resulted in the loss of nitrate-induced Ca2+ signature (primary nitrate responses) and retarded root growth, reminiscent to the phenotype observed in the nrt1.1 mutant. We further showed that CNGC15 was an active Ca2+-permeable channel that physically interacted with NRT1.1 protein in the plasma membrane. Importantly, CNGC15-NRT1.1 interaction silenced the channel activity of the heterocomplex that dissociated upon the rise in nitrate levels leading to re-activation of the CNGC15 channel. The dynamic interactions between CNGC15 and NRT1.1 therefore controlled the channel activity and Ca2+-influx in a nitrate-dependent manner. This study provides a new mechanism for nutrient-sensing that utilizes a nutrient transceptor-channel assembly to couple nutrient status to specific Ca2+ signature.