Abstract

Ethylene is a gaseous plant hormone that regulates plant growth, development, and stress adaptation, yet the molecular mechanism by which ethylene receptors perceive the hormone and initiate downstream signaling remains poorly understood. In this study, using genetic analyses in Arabidopsis thaliana , we reveal that the two ethylene receptor subfamilies do not act in parallel: subfamily I receptors constitute the core ethylene-sensing module, whereas subfamily II receptors require subfamily I receptors to function. Moreover, we show that subfamily I ethylene receptors are required for the rapid phase I growth inhibition that occurs within minutes of ethylene exposure, suggesting the involvement of a fast signaling mechanism. Using electrophysiological assays in Xenopus oocytes and mammalian human HEK293F cells, we reveal that only subfamily I ethylene receptors exhibit Ca 2+ permeability. The N-terminal residues of the subfamily I receptor ETHYLENE RESPONSE 1 (ETR1), including Cys65 and Phe76, are essential for this Ca 2+ permeability. Furthermore, ethylene promotes ETR1 Ca 2+ permeability in the Xenopus oocyte system and induces cytosolic Ca 2+ influx in plants in a manner dependent on subfamily I ethylene receptors. Collectively, our work supports a mechanistic framework in which subfamily I ethylene receptors integrate ethylene sensing with calcium influx, providing new insight into how plants translate hormonal cues into downstream signaling events.