J Integr Plant Biol. ›› 2022, Vol. 64 ›› Issue (4): 942-957.DOI: 10.1111/jipb.13239

• Plant-abiotic Interactions • Previous Articles    

Nitrate transporter NRT1.1 and anion channel SLAH3 form a functional unit to regulate nitrate-dependent alleviation of ammonium toxicity

Chengbin Xiao1, Doudou Sun1,2, Beibei Liu1, Xianming Fang1, Pengcheng Li1, Yao Jiang1, Mingming He1, Jia Li1,3, Sheng Luan4 and Kai He1*   

  1. 1 Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, China
    2 School of Life Sciences, Henan Agricultural University, Zhengzhou 450000, China
    3 School of Life Sciences, Guangzhou University, Guangzhou 510006, China
    4 Department of Plant and Microbial Biology, University of California, Berkeley 94720, CA, USA

    *Correspondence: Kai He (hekai@lzu.edu.cn)
  • Received:2022-01-15 Accepted:2022-02-27 Online:2022-03-01 Published:2022-04-01


Ammonium (NH4+) and nitrate (NO3) are major inorganic nitrogen (N) sources for plants. When serving as the sole or dominant N supply, NH4+ often causes root inhibition and shoot chlorosis in plants, known as ammonium toxicity. NO3 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 NO3 efflux channel SLAH3 is involved in this process. However, whether additional components contribute to NO3-mediated NH4+ detoxification is unknown. Previously, mutations in NO3 transporter NRT1.1 were shown to cause enhanced resistance to high concentrations of NH4+. Whereas, in this study, we found when the high-NH4+ medium was supplemented with low concentrations of NO3, nrt1.1 mutant plants showed hyper-sensitive phenotype instead. Furthermore, mutation in NRT1.1 caused enhanced medium acidification under high-NH4+/low-NO3 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 NO3 influx while NRT1.1 influenced NO3 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 NO3 transport and balancing rhizosphere acidification.

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