Sensing endoplasmic reticulum redox state by ethylene receptors.
basic_science · Level V
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- Record sourced from PubMed, PMID 42054993.
- Also identified by DOI 10.1016/j.cell.2026.04.004.
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Abstract
Endoplasmic reticulum (ER) redox homeostasis is critical for ER functionality and is implicated in various human diseases, yet its physiological significance in plants remains largely elusive. Ethylene, a key phytohormone, is perceived and transduced at the ER, suggesting an underexplored connection between the ER and ethylene signaling. Here, we show that ethylene receptors sense the ER redox state via lumen-localized intermolecular disulfide bonds. ER reductive stress, rather than ethylene, disrupts the disulfide-linked dimers of the receptors, repressing their function and thereby activating downstream ethylene signaling. Moreover, modulating disulfide bond formation in the receptor ETHYLENE RESPONSE 1 (ETR1) through ER redox shifts supports plant resilience under hypoxia and during photomorphogenesis. Finally, our findings suggest that sensing ER redox may be an ancestral receptor function, predating the substantial emergence of ethylene biosynthesis. This study illuminates a deeper nexus between organelle homeostasis and hormone signaling.