Abstract：
Rapeseed (Brassica napus L.) is extremely sensitive to excessive NH4+ toxicity. There remains incomplete knowledge of the causal factors behind the growth suppression in NH4+-nourished plants, with limited studies conducted specifically on field crop plants. In this study, we found that NH4+ toxicity significantly increased salicylic acid (SA) accumulation by accelerating the conversion of SA precursors. Moreover, exogenous SA application significantly aggravated NH4+ toxicity symptoms in the rapeseed shoots. Genome-wide differential transcriptomic analysis showed that NH4+ toxicity increased the expression of genes involved in the biosynthesis, transport, signaling transduction, and conversion of SA. SA treatment significantly increased shoot NH4+ concentrations by reducing the activities of glutamine synthase and glutamate synthase in NH4+-treated rapeseed plants. The application of an SA biosynthesis inhibitor, ABT, alleviated NH4+ toxicity symptoms. Furthermore, SA induced putrescine (Put) accumulation, resulting in an elevated ratio of Put to [spermidine (Spd) + spermine (Spm)] in the NH4+-treated plants, while the opposite was true for ABT. The application of exogenous Put and its biosynthesis inhibitor DFMA induced opposite effects on NH4+ toxicity in rapeseed shoots. These results indicated that the increased endogenous SA contributed noticeably to the toxicity caused by the sole NH4+-N supply in rapeseed shoots. This study provided fresh perspectives on the mechanism underlying excessive NH4+-induced toxicity and the corresponding alleviating strategies in plants.
摘要：
油菜（BrassicanapusL.）对过量的NH4毒性极为敏感。对NH4营养植物生长抑制背后的因果因素仍然不完全了解，专门对大田作物进行的有限研究。在这项研究中,我们发现NH4+毒性通过加速水杨酸（SA）前体的转化而显着增加了SA的积累。此外，外源SA的施用明显加重了油菜芽中NH4+的毒性症状。全基因组差异转录组分析表明，NH4+毒性增加了参与生物合成的基因的表达，运输,信号转导，和SA的转换。SA处理通过降低NH4处理的油菜籽植物中谷氨酰胺合酶和谷氨酸合酶的活性来显着增加芽NH4浓度。SA生物合成抑制剂的应用，ABT,缓解NH4+毒性症状。此外，SA诱导的腐胺（Put）积累，导致在NH4处理的植物中Put与[亚精胺（Spd）精胺（Spm）]的比例升高，而ABT则相反。外源Put及其生物合成抑制剂DFMA的应用对油菜芽中的NH4毒性产生了相反的影响。这些结果表明，内源性SA的增加显着导致油菜芽中唯一的NH4-N供应引起的毒性。这项研究为植物中过量NH4诱导毒性的机制和相应的缓解策略提供了新的视角。
