CML23 mediates NO induced Ca2+ signaling during hypocotyl elongation in Arabidopsis.

Calcium ions (Ca2+) play essential roles in plants, serving as both structural elements in cells and critical secondary messengers that influence growth, development, and stress adaptation. Similarly, nitric oxide (NO), a gaseous signaling molecule widespread in living organisms, participates in the regulation of diverse plant physiological processes. These two signaling molecules engage in a bidirectional interaction network, yet the molecular basis of their crosstalk remains largely unclear. Our earlier RNA-seq analysis revealed that CML23 expression in Arabidopsis seedlings is modulated by exogenous NO, leading us to propose that NO might suppress hypocotyl elongation by activating Ca2+ signaling through CML23. To investigate this hypothesis, we utilized Arabidopsis as a model system and combined genetic, biochemical, and molecular biology approaches to explore CML23's function in NO-mediated hypocotyl growth inhibition. Results showed that NO treatment strongly inhibited hypocotyl elongation in wild-type but had minimal effect in cml23 mutant. NO exposure induced post-translational S-nitrosylation and affected Ca2+-binding ability of CML23. Additionally, cytoplasmic Ca2+ levels in cml23 displayed diminished responsiveness to NO compared to the wild type. Transcriptomic profiling further indicated that CML23 contributes to the integration of NO-Ca2+ signaling with light and phytohormone pathways. This study enhances our comprehension of the NO-Ca2+ interaction network in plants.