Protons (H+) in acidic soils arrest plant growth. However, the mechanisms by which plants optimize their biological processes to diminish the unfavorable effects of H+ stress remain largely unclear. Here, we showed that in the roots of Arabidopsis thaliana, the C2H2-type transcription factor STOP1 in the nucleus was enriched by low pH in a nitrate-independent manner, with the spatial expression pattern of NITRATE TRANSPORTER 1.1 (NRT1.1) established by low pH required the action of STOP1. Additionally, the nrt1.1 and stop1 mutants, as well as the nrt1.1 stop1 double mutant, had a similar hypersensitive phenotype to low pH, indicating that STOP1 and NRT1.1 function in the same pathway for H+ tolerance. Molecular assays revealed that STOP1 directly bound to the promoter of NRT1.1 to activate its transcription in response to low pH, thus upregulating its nitrate uptake. This action improved the nitrogen use efficiency (NUE) of plants and created a favorable rhizospheric pH for root growth by enhancing H+ depletion in the rhizosphere. Consequently, the constitutive expression of NRT1.1 in stop1 mutants abolished the hypersensitive phenotype to low pH. These results demonstrate that STOP1-NRT1.1 is a key module for plants to optimize NUE and ensure better plant growth in acidic media.

中文翻译：

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STOP1 激活 NRT1.1 介导的硝酸盐吸收，为植物适应酸度创造有利的根际 pH 值

酸性土壤中的质子 (H+) 会阻止植物生长。然而，植物优化其生物过程以减少 H+ 胁迫的不利影响的机制仍不清楚。在这里，我们发现在拟南芥的根中，细胞核中的 C2H2 型转录因子 STOP1 在低 pH 条件下以不依赖硝酸盐的方式富集，其 NITRATE TRANSPORTER 1.1 (NRT1.1) 的空间表达模式由低 pH 值需要 STOP1 的作用。此外，nrt1.1 和 stop1 突变体以及 nrt1.1 stop1 双突变体对低 pH 具有相似的过敏表型，表明 STOP1 和 NRT1.1 在 H+耐受性的相同途径中发挥作用。分子分析显示 STOP1 直接与 NRT1.1 的启动子结合以激活其转录以响应低 pH 值，从而上调其对硝酸盐的吸收。这一作用提高了植物的氮利用效率 (NUE)，并通过增强根际 H+ 消耗为根系生长创造了有利的根际 pH 值。因此，NRT1.1 在 stop1 突变体中的组成型表达消除了对低 pH 值的过敏表型。这些结果表明，STOP1-NRT1.1 是植物优化 NUE 并确保植物在酸性介质中更好生长的关键模块。