Kinase SnRK1.1 regulates nitrate channel SLAH3 engaged in nitrate-dependent alleviation of ammonium toxicity

• DOI: 10.1093/plphys/kiab057
• Publication Date: 2021-02-08T21:02:30Z
• Authors: Doudou Sun; Xianming Fang; Chengbin Xiao; Zhen Ma; Xuemei Huang; Jingrong Su; Jia Li; Jiafeng Wang; Suomin Wang; Sheng Luan; Kai He
• Keywords: Ammonium nitrate

Nitrate (NO3-) and ammonium (NH4+) are major inorganic nitrogen (N) supplies for plants, but NH4+ as the sole or dominant N source causes growth inhibition in many known toxicity. Small amounts of NO3- can significantly mitigate toxicity, anion channel SLAC1 homolog 3 (SLAH3) is involved this process, mechanistic detail how SLAH3 regulates nitrate-dependent alleviation toxicity still largely unknown. In study, we identified SnRK1.1, a central regulator energy homeostasis, various stress responses, interactor Arabidopsis (Arabidopsis thaliana). Our results suggest that SNF1-related protein kinase 1 (SnRK1.1) functions negative SLAH3. Kinase assays indicate SnRK1.1 strongly phosphorylates C-terminal at site S601. Under high-NH4+/low-pH condition, phospho-mimetic phospho-dead mutations S601 result barely rescued phenotypes fully complemented slah3. Furthermore, migrates from cytoplasm to nucleus under conditions. The translocation cytosol high-ammonium releases on SLAH3, which allows SLAH3-mediated efflux leading stress. study reveals phosphorylation also plays important role regulation provides additional insights into plants.