Autophagic degradation of EIN3 ensures developmental plasticity and recovery from environmental stress in Arabidopsis

Abstract

Ethylene signaling, mediated by the key transcription factor EIN3, regulates diverse developmental processes and stress adaptations, including hypocotyl growth, aging, and submergence tolerance. Autophagy, a cellular recycling process, also facilitates adaptation by reprogramming cellular components. While EIN3 degradation via the proteasome is well established, its connection to autophagy remains unclear. Here, we show that EIN3 turnover is directly regulated by ATG8-mediated autophagy. Consistently, autophagy-deficient plants exhibit impaired EIN3-dependent hypocotyl growth during light-to-dark transitions. Additionally, EIN3 accumulation contributes to the premature senescence observed in atg mutants. Beyond development, our combination of cell imaging, phenotypic analyses, and proteomics reveals that autophagy is essential for EIN3-driven transcriptional reprogramming during submergence. Together, our findings uncover a direct role for autophagy in regulating EIN3 stability, providing mechanistic insight into how this process fine-tunes ethylene responses in growth and stress adaptation.