Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5
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+ transloc...
| Autores principales: | , , , , , |
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| Formato: | Journal Article |
| Lenguaje: | Inglés |
| Publicado: |
Wiley
2021
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| Materias: | |
| Acceso en línea: | https://hdl.handle.net/10568/164192 |
| _version_ | 1855533155273932800 |
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| author | Chen, Haifei Zhang, Quan Wang, Xueru Zhang, Jianhua Ismail, Abdelbagi M. Zhang, Zhenhua |
| author_browse | Chen, Haifei Ismail, Abdelbagi M. Wang, Xueru Zhang, Jianhua Zhang, Quan Zhang, Zhenhua |
| author_facet | Chen, Haifei Zhang, Quan Wang, Xueru Zhang, Jianhua Ismail, Abdelbagi M. Zhang, Zhenhua |
| author_sort | Chen, Haifei |
| collection | Repository of Agricultural Research Outputs (CGSpace) |
| description | 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. |
| format | Journal Article |
| id | CGSpace164192 |
| institution | CGIAR Consortium |
| language | Inglés |
| publishDate | 2021 |
| publishDateRange | 2021 |
| publishDateSort | 2021 |
| publisher | Wiley |
| publisherStr | Wiley |
| record_format | dspace |
| spelling | CGSpace1641922025-01-24T14:20:08Z Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 Chen, Haifei Zhang, Quan Wang, Xueru Zhang, Jianhua Ismail, Abdelbagi M. Zhang, Zhenhua plant science physiology 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. 2021-12 2024-12-19T12:53:35Z 2024-12-19T12:53:35Z Journal Article https://hdl.handle.net/10568/164192 en Wiley Chen, Haifei; Zhang, Quan; Wang, Xueru; Zhang, Jianhua; Ismail, Abdelbagi M. and Zhang, Zhenhua. 2021. Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5. Plant Cell and Environment, Volume 44 no. 12 p. 3806-3818 |
| spellingShingle | plant science physiology Chen, Haifei Zhang, Quan Wang, Xueru Zhang, Jianhua Ismail, Abdelbagi M. Zhang, Zhenhua Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title | Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title_full | Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title_fullStr | Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title_full_unstemmed | Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title_short | Nitrogen form-mediated ethylene signal regulates root-to-shoot K+ translocation via NRT1.5 |
| title_sort | nitrogen form mediated ethylene signal regulates root to shoot k translocation via nrt1 5 |
| topic | plant science physiology |
| url | https://hdl.handle.net/10568/164192 |
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