A research team led by Prof. Hongquan Yang from the College of Life Sciences at Shanghai Normal University has published a groundbreaking study in Molecular Plant titled:
“Gibberellin triggers ATG8-dependent autophagic degradation of DELLA proteins to promote seed germination and skotomorphogenesis under nutrient starvation in Arabidopsis.”
This study uncovers the molecular mechanism by which gibberellin (GA) induces autophagic degradation of DELLA proteins, thereby promoting seed germination and skotomorphogenesis under nutrient-starved dark conditions.
During the experiments, seeds were cultivated in the JIUPO Plant Growth Chamber BPC500DH, where precise environmental parameters and lighting conditions were maintained. The findings reveal how the plant hormone GA strategically “hijacks” the intracellular autophagy system under nutrient-deficient darkness to stimulate growth—offering new insights into plant adaptive strategies under environmental stress.
Under carbon and nitrogen starvation (-C-N) in darkness:
- Wild-type (WT) seed germination rates increased sharply with rising GA concentration.
- In contrast, the autophagy-defective double mutant atg5 atg7 showed almost no response to GA.
- Similarly, the atg8n mutant (lacking all nine ATG8 family members) displayed GA insensitivity.
These genetic data strongly demonstrate that GA-promoted seed germination and hypocotyl elongation under nutrient starvation strictly depend on a functional autophagy pathway.
Further genetic analysis using the atg5 atg7 rgl2 triple mutant revealed germination rates comparable to the rgl2 single mutant. This indicates that RGL2 (a key DELLA protein) functions downstream of ATG5/ATG7, forming a clear regulatory cascade:
GA → Autophagy → RGL2 degradation → Germination
Under nutrient starvation and darkness:
GA binds to its receptor GID1 → recruits ATG8 → forms a ternary complex with DELLA proteins → facilitates autophagosome formation → transports DELLA proteins to the vacuole for degradation → releases growth repression → promotes germination and elongation.
Using GFP-tagged DELLA proteins (RGL2 and RGA), researchers observed:
- Under normal conditions, DELLA proteins localize in the nucleus.
- Under -C-N + GA treatment, DELLA proteins exit the nucleus, form cytoplasmic puncta, co-localize with autophagosome marker mCherry-ATG8, and are eventually transported to the vacuole.
- This process is blocked in the gid1ac mutant.
Based on these findings, the researchers proposed a new working model explaining how plants flexibly switch protein degradation pathways depending on environmental nutrient status.
This study represents a major conceptual advance:
• A newly identified degradation pathway – First evidence that GA can degrade DELLA proteins via autophagy, challenging the previous paradigm centered solely on the 26S proteasome pathway.
• A novel molecular bridge – Discovery that GA receptor GID1 directly connects hormone signaling with the autophagy machinery.
• Profound biological implications – Demonstrates how plants optimize resource allocation under stress (darkness and starvation) by activating autophagy to amplify GA signaling and accelerate growth, enhancing survival competitiveness.
About the Authors
Co-first authors:
Shilong Zhang and Lu Jiang (PhD candidates, College of Life Sciences, Shanghai Normal University)
Co-corresponding authors:
Prof. Hongquan Yang and Associate Prof. Wenxiu Wang
The research was supported by the National Key R&D Program of China, the National Natural Science Foundation of China, the Shanghai Key Laboratory of Molecular Plant Sciences, and the Shanghai Center for Plant Germplasm Resources.