铵根离子和硝酸根离子是植物重要无机氮源。铵根离子作为唯一或优势无机氮源时通常会对植物生长产生抑制，称为铵毒。硝酸根离子可以有效地缓解铵毒，其分子机理未知。我们前期的工作发现铵毒的产生与高铵条件下植物对根际的迅速酸化有关；同时揭示了拟南芥根中的一个硝酸根离子通道蛋白SLAH3，参与了抗高铵与适应酸性环境过程。目前的工作鉴定到一个蛋白激酶SnRK1.1，结合并磷酸化SLAH3的C端。初步的遗传学实验结果表明SnRK1.1可能通过负调节SLAH3参与抗铵毒、低pH的过程。同时发现豆科植物蒺藜苜蓿中存在SLAH3的同源基因，其中部分基因的表达可以恢复拟南芥slah3突变体表型，说明SLAH3在拟南芥和苜蓿中功能具有保守性。本项目旨在已获得的研究基础上，揭示SnRK1.1如何调控SLAH3，参与抗高铵、低pH的过程，揭示SLAH3相关调控网络的详细分子机理；同时揭示蒺藜苜蓿中SLAH3的生物学功能。

Ammonium and nitrate are essential inorganic nitrogen source for plants. However, when ammonium becomes the sole or dominant inorganic nitrogen source, it inhibits the growth of plants, known as ammonium toxicity. Nitrate can effectively alleviate ammonium toxicity, the molecular mechanism of which is unknown. Our previous work indicated that ammonium toxicity is likely caused by rapid acidification of rhizosphere upon high ammonium condition. We also found a gene SLAH3, encoding a nitrate efflux channel in Arabidopsis root, is involved in regulating high ammonium and low pH stresses. Our current study identified a protein kinase SNRK1.1 that interacts with and strongly phosphorylates the C terminal of SLAH3. Genetic results suggested that SNRK1.1 negatively regulates SLAH3 in dealing with high ammonium and low pH conditions. We also found that the genome of Medicago truncatula contains homologs of AtSLAH3. The expression of several MtSLAH3 was able to rescue the phenotype of Arabidopsis slah3 mutant, suggesting the function of SLAH3 is conserved in Medicago and Arabidopsis. Based on our preliminary genetic and biochemical results, the current project proposes to reveal how SNRK1.1 regulates SLAH3 in regulating adaption of high ammonium and low pH, and ultimately to elucidate the molecular mechanisms of SLAH3 in Arabidopsis as well as in Medicago truncatula.