CIPK15-Mediated Inhibition of Nh <sub>4</sub> <sup> </sup> Transport Protects Arabidopsis From Submergence

Ammonium (Nh4+) is a key nitrogen form used by plants and becomes toxic once at high level of accumulation. Toxicity is aggravated under hypoxic/anaerobic conditions, e.g., during flooding or submergence, due to reduced assimilation capacity. AMT1;1 transporter mediate NH4+ uptake into roots. Under conditions of oxygen-deficiency, i.e., submergence, the CBL-interacting protein kinase OsCIPK15 triggers SnRK1A signaling, promoting starch mobilization, thereby increasing availability of ATP, reduction equivalents and acceptors for Nh4+ assimilation in rice. Our previous study demonstrates that AtCIPK15 phosphorylates AMT1;1 whose activity is under allosteric feedback control by phosphorylation of T460 in the cytosolic C-terminus. Here we showed that submergence caused higher Nh4+accumulation in wild type, but not nitrate or in AMT1s transporters knock-out mutants. In addition, submergence triggered rapid AtAMT1;1 and AtCIPK15 transcripts and AMT1 phosphorylation accumulation. Notably, cipk15 knock-outmutants showed no increased in AMT1 phosphorylation and were hypersensitive to submergence. The data indicate that under submergence conditions, CIPK15 inhibits AMT activity to limit Nh4+-accumulation in conditions where Nh4+-assimilation capacity is impaired, while increasing assimilation capacity.