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Ansboel, J.

Publications and source records attributed to Ansboel, J..

2 recordsLinked to original sources

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

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.

plant biology↗

Autophagy regulates ARF7 degradation to facilitate root branching

Auxin dictates root architecture via the Auxin Response Factor (ARF) family of transcription factors, which control lateral root (LR) formation. In Arabidopsis, ARF7 regulates the specification of prebranch sites (PBS) generating LRs through gene expression oscillations and plays a pivotal role during LR initiation. Despite the importance of ARF7 in this process, there is a surprising lack of knowledge about how ARF7 turnover is regulated and how this impacts root architecture. Here, we show that ARF7 accumulates in autophagy mutants and is degraded through NBR1-dependent selective autophagy. We demonstrate that the previously reported rhythmic changes to ARF7 abundance in roots are modulated via autophagy and might occur in other tissues. Additionally, we prove that the level of co- localization between ARF7 and autophagy markers oscillates and can be modulated by auxin to trigger ARF7 turnover. Furthermore, we observed that autophagy impairment prevents ARF7 oscillation and reduces both PBS establishment and LR formation. In conclusion we report a novel role for autophagy during development, namely by enacting auxin-induced selective degradation of ARF7 to optimize periodic root branching.

plant biology↗