The coordinated utilization of nitrogen (N) and phosphorus (P) is vital for plants to maintain nutrient balance and achieve optimal growth. Previously, we revealed a mechanism by which nitrate induces genes for phosphate utilization; this mechanism depends on NRT1.1B-facilitated degradation of cytoplasmic SPX4, which in turn promotes cytoplasmic-nuclear shuttling of PHR2, the central transcription factor of phosphate signaling, and triggers the nitrate-induced phosphate response (NIPR) and N-P coordinated utilization in rice. In this study, we unveiled a fine-tuning mechanism of NIPR in the nucleus regulated by Highly Induced by Nitrate Gene 1 (HINGE1, also known as RLI1), a MYB-transcription factor closely related to PHR2. RLI1/HINGE1, which is transcriptionally activated by PHR2 under nitrate induction, can directly activate the expression of phosphate starvation-induced genes. More importantly, RLI1/HINGE1 competes with PHR2 for binding to its repressor proteins in the nucleus (SPX proteins), and consequently releases PHR2 to further enhance phosphate response. Therefore, RLI1/HINGE1 amplifies the phosphate response in the nucleus downstream of the cytoplasmic SPX4-PHR2 cascade, thereby enabling fine-tuning of N-P balance when nitrate supply is sufficient.

氮（N）和磷（P）的协调利用对于植物维持养分平衡和实现最佳生长至关重要。以前，我们揭示了硝酸盐诱导磷酸盐利用基因的机制；该机制依赖于 NRT1.1B 促进细胞质 SPX4 的降解，进而促进 PHR2（磷酸盐信号转导的中心转录因子）的细胞质 - 核穿梭，并触发水稻中硝酸盐诱导的磷酸盐反应（NIPR）和 NP 协同利用. 在这项研究中，我们揭示了 NIPR 在受硝酸盐基因 1 高度诱导（HINGE1，也称为 RLI1）（一种与 PHR2 密切相关的 MYB 转录因子）调控的细胞核中的微调机制。RLI1/HINGE1，在硝酸盐诱导下被 PHR2 转录激活，可直接激活磷饥饿诱导基因的表达。更重要的是，RLI1/HINGE1 与 PHR2 竞争结合其细胞核中的阻遏蛋白（SPX 蛋白），从而释放 PHR2 以进一步增强磷酸盐反应。因此，RLI1/HINGE1 放大了细胞质 SPX4-PHR2 级联下游细胞核中的磷酸盐反应，从而在硝酸盐供应充足时能够微调 NP 平衡。