The gaseous plant hormone ethylene (ET) regulates diverse growth responses and adaptive processes to environmental stimuli. Although the role of ET in stress signalling is well established, its effects on stomatal responses remain paradoxical. ET induces stomatal closure in some contexts yet antagonizes abscisic acid‐mediated closure in others. While diverse studies have reported that ET regulates stomatal responses, the differential role of ET in stomatal signalling has not been reconciled into a unified framework. Here, we synthesize current evidence into a bidirectional model of ET‐dependent stomatal regulation, in which ET signalling produces two antagonistic outputs: a closure pathway driven by Gα‐dependent, RBOHD/F‐mediated H 2 O 2 production and downstream NO and H 2 S signals acting via SLAC1‐type anion channels; and an opposing pathway in which EIN2‐dependent flavonol accumulation scavenges guard‐cell ROS, thereby antagonizing stomatal closure. Additionally, the differential role of ET across species, dosages and stress conditions, as well as the compensatory role of ET in stomatal closure when ABA signalling is compromised is also discussed. This review offers novel insights into the function of ET in stomatal regulation and provides a mechanistic foundation for harnessing ET signalling to optimize the trade‐off between plant growth and stress resilience.
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Khan et al. (2026) studied this question.
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