Over-expression transcription factor ERF1 promotes seed germination by enhancing mitochondrial function

ERF1 modulates mitochondrial function to fine-tune ROS homeostasis and suppress ABA signaling, thereby facilitating seed germination. Seed germination represents a critical phase in the plant life cycle, and its proper regulation is crucial for optimizing crop productivity. Mitochondria are essential organelles that provide energy for seed germination in plants. However, how mitochondria fine-tune seed germination remains poorly understood. In this study, we demonstrated that ETHYLENE RESPONSE FACTOR 1 (ERF1), a key transcription factor in the canonical ethylene signaling pathway, promotes seed germination by enhancing mitochondrial function. Through the integration of gene expression, physiological and biochemical characterization, and germination analyses, we revealed that overexpression of ERF1 strengthened mitochondrial function, thereby reducing reactive oxygen species (ROS) accumulation and facilitating seed germination. Moreover, we demonstrated that overexpression of ERF1 repressed the ABA signaling pathway by inhibiting the mitochondrial retrograde signaling (MRS) pathway, thereby reducing ROS levels via downregulation of RBOHD expression and activity and enhancing sugar supply, which finally promoted seed germination. These results provide new insights into how ERF1 modulates mitochondrial function to fine-tune ROS homeostasis and suppress ABA signaling during seed germination. This work provides valuable mechanistic insights and lays the groundwork for future strategies aiming at improving seed germination in agricultural crops.