BIN2 phosphorylation of GRF5 suppresses low-nitrate root foraging by inhibiting transcriptional activity and UBP12/13-mediated deubiquitination

Root developmental plasticity enables plants to adapt to nutrient-deficient conditions. Under low-nitrate (LN) conditions, enhanced exploratory root growth-characterized by increased primary and lateral root (LR) elongation-facilitates nutrient foraging. Although nitrate-hormone crosstalk regulates this process, the underlying molecular mechanisms remain poorly understood. Here, we identify the BIN2-GRF5-UBP12/13 module that governs root foraging responses to LN in Arabidopsis. We demonstrate that BIN2 phosphorylates GRF5 at Ser205, thereby reducing its stability and transcriptional activity. Integrative DAP-seq and transcriptomic analyses reveal that GRF5 directly regulates key nitrate-responsive genes, including the dual-affinity transporter gene NRT1.1 and the high-affinity uptake gene NRT2.1. Furthermore, dephosphorylated GRF5 preferentially interacts with UBIQUITIN-SPECIFIC PROTEASES 12 and 13 (UBP12/13), which stabilizes GRF5 and promotes LR elongation under LN conditions. Our findings delineate a phosphorylation-dependent regulatory circuit that fine-tunes root foraging adaptation, advancing the mechanistic understanding of nitrate sensing in plants.