Nitrogen form‐mediated ethylene signal regulates root‐to‐shoot K<sup>+</sup> translocation via <i><scp>NRT1</scp>.5</i>
Haifei Chen, Quan Zhang, Xueru Wang, Jianhua Zhang, Abdelbagi M. Ismail, Zhenhua Zhang
Abstract
Abstract 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 NO 3 − and NH 4 + on root‐shoot K + translocation were due to differential regulation of an ethylene signalling pathway targeting the NRT1.5 transporter. NH 4 + upregulated the transcriptional activity of EIN3, but repressed the expression of NRT1.5 . However, the addition of NO 3 − 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 NH 4 + 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 .