Nitrogen form‐mediated ethylene signal regulates root‐to‐shoot K+ translocation via NRT1.5

• Published in: Plant, cell and environment cell and environment, 2021-12, Vol.44 (12), p.3576-3588
• Main Authors: Chen, Haifei, Zhang, Quan, Wang, Xueru, Zhang, Jianhua, Ismail, Abdelbagi M., Zhang, Zhenhua
• Format: Article
• Language: English
• Subjects: Anion Transport Proteins - genetics; Anion Transport Proteins - metabolism; Arabidopsis; Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Chlorosis; Ethylene; Ethylenes - metabolism; Homeostasis; leaf senescence; Mutants; N form; nitrate transport; Nitrogen; Nitrogen - metabolism; Phenotypes; Plant Roots - metabolism; Plant Shoots - metabolism; Potassium; Potassium - metabolism; root‐to‐shoot K+ translocation; Signal transduction; Transcription; Translocation
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1111/pce.14182

Nitrogen–potassium synergistic and antagonistic interactions are the typical case of nutrient interactions. However, the underlying mechanism for the integration of the external N form into K+ homeostasis remains unclear. Here, we show that opposite effects of NO3− and NH4+ on root‐shoot K+ translocation were due to differential regulation of an ethylene signalling pathway targeting the NRT1.5 transporter. NH4+ upregulated the transcriptional activity of EIN3, but repressed the expression of NRT1.5. However, the addition of NO3− strongly suppressed the activity of EIN3, whereas its addition upregulated the expression of AtNRT1.5 and shoot K+ concentration. The 35S:EIN3/ein3eil1 plants, nrt1.5 mutants and nrt1.5/skor double mutants displayed a low K+ chlorosis phenotype, especially under NH4+ conditions with low K+ supply. Ion content analyses indicate that root‐to‐shoot K+ translocation was significantly reduced in these mutants. A Y1H assay, an EMSA and a transient expression assay confirmed that AtEIN3 protein could directly bind to the promoter of NRT1.5 to repress its expression. Furthermore, grafted plants with the roots of 35S:EIN3 and ein3eil1/nrt1.5 mutants displayed marked leaf chlorosis with a low K+ concentration. Collectively, our findings reveal that the interaction between N form and K+ was achieved by modulating root‐derived ethylene signals to regulate root‐to‐shoot K+ translocation via NRT1.5. Nitrogen‐potassium synergistic and antagonistic interactions are the typical case of nutrient interactions. K synergistic and antagonistic interactions were determined by the form of available N. This study supports a model for the interaction between N forms and K translocation from roots to shoots. In the presence of NH4+, NH4+ nutrition enhanced the biosynthesis of ET and the transcriptional activity of EIN3, which subsequently repressed the expression of AtNRT1.5, resulting in severe shoot K+ deficiency and early leaf senescence. However, the supply of low amounts of NO3− strongly suppressed the activity of EIN3 and significantly increased AtNRT1.5 expression and shoot K+ concentration. Thus, NO3− possibly acts as a signaling molecule that alleviates NH4+ toxicity, and this is at least partially dependent on its tight regulation of ET production. Collectively, the present study established a regulation pathway to explain the interaction between N form and K+ translocation, and showed that N form‐mediated ethylene signal regulated root‐to‐shoot K+