Abstract
Covering 40-50% of world's arable lands, acidic soils pose a major constraint on global crop productivity by severely restricting root development and nutrient acquisition. The Arabidopsis C2H2-type transcription factor STOP1 plays a fundamental role in mitigating acid stress by activating H(+)/NO(3)(-) symport via NRT1.1, thereby driving rhizosphere alkalinization to protect root growth and improving nitrogen use efficiency (NUE). However, the upstream regulation of this pH-responsive STOP1-NRT1.1 pathway remains poorly defined. Here, we identify the central SWI2/SNF2-type ATPase BRAHMA (BRM) as a key suppressor of the STOP1 pathway. BRM physically interacts with STOP1 and occupies the genomic region of NRT1.1, repressing the STOP1-dependent activation of NRT1.1 expression and consequently limiting NO(3)(-) uptake and rhizosphere alkalization under chronic acidity. Genetic epistasis analysis using brm stop1 and brm nrt1.1 double mutants establish BRM as an upstream regulator of this signaling module. Notably, low pH rapidly triggers BRM degradation independent of NO(3)(-) availability, thereby relieving its repression on the STOP1-NRT1.1 pathway. This dynamic BRM disintegration enables robust induction of H(+)-coupled NO(3)(-) uptake, remodeling the rhizosphere pH landscape to foster optimal root growth under acidity. Collectively, our findings uncover the BRM-STOP1-NRT1.1 axis as a central regulatory module integrating NO(3)(-) acquisition with pH homeostasis, offering a dual-benefit strategy for enhancing crop resilience to acid soils and reducing fertilizer-driven acidification through improved NUE.