Nitrate transporter NRT1.1 and anion channel SLAH3 form a functional unit to regulate nitrate‐dependent alleviation of ammonium toxicity
Chengbin Xiao, Doudou Sun, Beibei Liu, Xianming Fang, Pengcheng Li, Yao Jiang, Mingming He, Jia Li, Sheng Luan, Kai He
Abstract
Abstract Ammonium (NH 4 + ) and nitrate (NO 3 − ) are major inorganic nitrogen (N) sources for plants. When serving as the sole or dominant N supply, NH 4 + often causes root inhibition and shoot chlorosis in plants, known as ammonium toxicity. NO 3 − usually causes no toxicity and can mitigate ammonium toxicity even at low concentrations, referred to as nitrate‐dependent alleviation of ammonium toxicity. Our previous studies indicated a NO 3 − efflux channel SLAH3 is involved in this process. However, whether additional components contribute to NO 3 − ‐mediated NH 4 + detoxification is unknown. Previously, mutations in NO 3 − transporter NRT1.1 were shown to cause enhanced resistance to high concentrations of NH 4 + . Whereas, in this study, we found when the high‐NH 4 + medium was supplemented with low concentrations of NO 3 − , nrt1.1 mutant plants showed hyper‐sensitive phenotype instead. Furthermore, mutation in NRT1.1 caused enhanced medium acidification under high‐NH 4 + /low‐NO 3 − condition, suggesting NRT1.1 regulates ammonium toxicity by facilitating H + uptake. Moreover, NRT1.1 was shown to interact with SLAH3 to form a transporter‐channel complex. Interestingly, SLAH3 appeared to affect NO 3 − influx while NRT1.1 influenced NO 3 − efflux, suggesting NRT1.1 and SLAH3 regulate each other at protein and/or gene expression levels. Our study thus revealed NRT1.1 and SLAH3 form a functional unit to regulate nitrate‐dependent alleviation of ammonium toxicity through regulating NO 3 − transport and balancing rhizosphere acidification.