Chen Yen-Ning, Ho Cheng-Hsun
Agricultural Biotechnology Research Center, Academia Sinica, Taipei, 115, Taiwan.
Heliyon. 2023 Sep 15;9(9):e20235. doi: 10.1016/j.heliyon.2023.e20235. eCollection 2023 Sep.
Ammonium (NH) serves as a vital nitrogen source for plants, but it can turn toxic when it accumulates in excessive amounts. Toxicity is aggravated under hypoxic/anaerobic conditions, e.g., during flooding or submergence, due to a lower assimilation capacity. AMT1; 1 mediates NH uptake into roots. Under conditions of oxygen-deficiency, i.e., submergence, the CBL-interacting protein kinase OsCIPK15 has been shown to trigger SnRK1A signaling, promoting starch mobilization, thereby the increasing availability of ATP, reduction equivalents and acceptors for NH assimilation in rice. Our previous study in Arabidopsis demonstrates that AtCIPK15 phosphorylates AMT1; 1 whose activity is under allosteric feedback control by phosphorylation of T460 in the cytosolic C-terminus. Here we show that submergence cause higher NH accumulation in wild-type, plant but not of nitrate, nor in a quadruple knock-out mutant. In addition, submergence triggers rapid accumulation of and transcripts as well as AMT1 phosphorylation. Significantly, knock-out mutants do not exhibit an increase in AMT1 phosphorylation; however, they do display heightened sensitivity to submergence. These findings suggest that CIPK15 suppresses AMT activity, resulting in decreased NH accumulation during submergence, a period when NH assimilation capacity may be impaired.
铵（NH）是植物重要的氮源，但过量积累时会产生毒性。在缺氧/厌氧条件下，如洪水或淹没期间，由于同化能力较低，毒性会加剧。AMT1;1介导铵进入根部。在缺氧条件下，即淹没时，已证明与CBL相互作用的蛋白激酶OsCIPK15会触发SnRK1A信号传导，促进淀粉动员，从而增加水稻中用于铵同化的ATP、还原当量和受体的可用性。我们之前在拟南芥中的研究表明，AtCIPK15使AMT1;1磷酸化，其活性受胞质C末端T460磷酸化的变构反馈控制。在这里，我们表明淹没导致野生型植物中铵积累增加，但硝酸盐不增加，在四重敲除突变体中也不增加。此外，淹没会触发 和 转录本以及AMT1磷酸化的快速积累。值得注意的是，敲除突变体的AMT1磷酸化没有增加；然而，它们对淹没表现出更高的敏感性。这些发现表明，CIPK15抑制AMT活性，导致淹没期间铵积累减少，而此时铵同化能力可能受损。
