STOP1 activates NRT1.1-mediated nitrate uptake to create a favorable rhizospheric pH for plant adaptation to acidity

背景回顾：Protons (H+) in acidic soils arrest plant growth. 

提出问题：However, the mechanisms by which plants optimize their biological processes to diminish the unfavorable effects of H+ stress remain largely unclear. 

结果1-诱导表达：Here, we showed that in the roots of Arabidopsis thaliana, the C2H2-type transcription factor STOP1 in the nucleus was enriched bylow 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. 

结果2-STOP1与NRT1.1：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. 

结果3-STOP1直接调控NRT1.1基因：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. 

结论：These results demonstrate that STOP1-NRT1.1 is a key module for plants to optimize NUE and ensure better plant growth in acidic media.

 摘 要 

酸性土壤中的氢离子会妨碍植物的正常生长。但是，植物采取何种机制来消除氢离子胁迫对于植物的有害影响还不清楚。本文中，作者发现在拟南芥的根中，低pH值会以硝酸盐非依赖性的方式诱导C2H2类转录因子STOP1在细胞核中富集，而低pH值需要依赖STOP1来建立硝酸盐转运蛋白编码基因NRT1.1的空间表达模式。另外，nrt1.1突变体和stop1突变体以及nrt1.1 stop1双突植株具有类似的对于低pH的超敏表型，说明STOP1和NRT1.1可能在同一个通路上发挥H+耐受性的功能。分子实验显示STOP1能够响应于低pH，直接结合到NRT1.1基因的启动子区，激活NRT1.1基因的转录，从而上调植株的硝酸盐吸收能力。该过程提升了植株对于氮的利用效率，并且通过加强根际的氢离子消耗，为根生长创造了有利的根际pH环境。因此，通过在stop1突变体中组成型表达NRT1.1消除了其对低pH的超敏表型。本文的研究结果表明，STOP1-NRT1.1是植物优化氮利用效率和确保在酸性介质中更好生长的关键模块。