SnRK1 orchestrates nitrogen remobilization by activating autophagy and repressing TOR during grain filling

Optimizing nitrogen use efficiency is paramount for global food security, particularly during the critical grain-filling stage when nitrogen must be remobilized from senescing tissues to developing seeds. This review establishes the SNF1-related protein kinase 1 (SnRK1) as the central regulator of this process. Current evidence establishes that SnRK1, activated by declining energy status, directly initiates a metabolic switch from anabolism to catabolism by orchestrating both carbon fluxes and nitrogen recycling machinery. It achieves this by two primary mechanisms: first, by directly activating autophagy-dependent degradation pathways to dismantle cellular components, and second, by repressing the growth-promoting Target of Rapamycin (TOR) kinase. This coordinated action effectively transforms senescing leaves into nutrient donors. We synthesize recent evidence from phosphoproteomics and interactomics to detail how SnRK1 complex assembly, its antagonism with TOR, and its direct phosphorylation of autophagic components drive nitrogen recycling. Furthermore, we explore how SnRK1 integrates hormonal and environmental signals to reprogram the transcriptome and metabolome, ensuring efficient nitrogen remobilization. Finally, we discuss the agronomic implications of targeting the SnRK1 signaling network for breeding crops with superior nitrogen use efficiency and yield.