Nitrate starvation inhibits stomatal opening via the long-distance CEP1-CEPR2 signaling cascade
Lingyan Wang, Siyu Chen, Wen Shi, Sijie Xing, Chao Han, Ming‐Yi Bai, Min Fan
Abstract
Carbon and nitrogen metabolisms are tightly coordinated to optimize plant growth. Stomata play critical roles in photosynthesis and carbon metabolism. However, the specific molecular mechanism by which nitrogen starvation affects stomatal movement is still fragmentary. Here, we demonstrate that nitrate starvation suppresses photosynthetic efficiency by inhibiting light-induced stomatal opening through the long-distance CEP1-CEPR2 signaling cascade, which is observed in multiple plant species. Exogenous application of CEP1 induced by nitrate starvation in the roots also inhibits light-induced stomatal opening. CEPR2, the receptor of CEPs, mediates these effects. Grafting and stomatal-specific expression of CEPR2 experiments highlight the necessity of CEPR2 in the shoot for the response. Furthermore, nitrate starvation and CEP1 treatment induce H 2 O 2 accumulation in guard cells through CEPR2, involving BIK1 and RBOHD. Overall, our findings reveal that nitrate starvation induces H 2 O 2 accumulation in guard cells through the long-distance CEP1-CEPR2-BIK1 signaling cascade, impeding light-induced stomatal opening and subsequently inhibiting photosynthesis.