Sun Tong, Wang Ting, Qiang Yalin, Zhao Gangqing, Yang Jian, Zhong Hua, Peng Xiaojue, Yang Jing, Li Yangsheng
State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan, China.
Department of Chemistry, University of Kentucky, Lexington, KY, United States.
Front Plant Sci. 2022 Apr 29;13:863283. doi: 10.3389/fpls.2022.863283. eCollection 2022.
Ammonium ( ) is one of the major nitrogen sources for plants. However, excessive ammonium can cause serious harm to the growth and development of plants, i.e., ammonium toxicity. The primary regulatory mechanisms behind ammonium toxicity are still poorly characterized. In this study, we showed that OsCIPK18, a CBL-interacting protein kinase, plays an important role in response to ammonium toxicity by comparative analysis of the physiological and whole transcriptome of the T-DNA insertion mutant () and the wild-type (WT). Root biomass and length of are less inhibited by excess compared with WT, indicating increased resistance to ammonium toxicity. Transcriptome analysis reveals that OsCIPK18 affects the uptake by regulating the expression of OsAMT1;2 and other transporters, but does not affect ammonium assimilation. Differentially expressed genes induced by excess in WT and were associated with functions, such as ion transport, metabolism, cell wall formation, and phytohormones signaling, suggesting a fundamental role for OsCIPK18 in ammonium toxicity. We further identified a transcriptional regulatory network downstream of OsCIPK18 under stress that is centered on several core transcription factors. Moreover, OsCIPK18 might function as a transmitter in the auxin and abscisic acid (ABA) signaling pathways affected by excess ammonium. These data allowed us to define an OsCIPK18-regulated/dependent transcriptomic network for the response of ammonium toxicity and provide new insights into the mechanisms underlying ammonium toxicity.
铵（ ）是植物主要的氮源之一。然而，过量的铵会对植物的生长发育造成严重危害，即铵毒。铵毒背后的主要调控机制仍不清楚。在本研究中，我们通过对T-DNA插入突变体（ ）和野生型（WT）的生理和全转录组进行比较分析，表明CBL相互作用蛋白激酶OsCIPK18在响应铵毒中起重要作用。与WT相比， 的根生物量和长度受过量 的抑制较小，表明其对铵毒的抗性增强。转录组分析表明，OsCIPK18通过调节OsAMT1;2和其他 转运蛋白的表达来影响 的吸收，但不影响铵同化。WT和 中过量 诱导的差异表达基因与离子运输、代谢、细胞壁形成和植物激素信号传导等功能相关，表明OsCIPK18在铵毒中起重要作用。我们进一步确定了在 胁迫下以几个核心转录因子为中心的OsCIPK18下游转录调控网络。此外，OsCIPK18可能在受过量铵影响的生长素和脱落酸（ABA）信号通路中作为信号传递者发挥作用。这些数据使我们能够定义一个由OsCIPK18调控/依赖的转录组网络来响应铵毒，并为铵毒的潜在机制提供新的见解。
