Summary Ammonium (NH4+) is toxic to root growth in most plants, even at moderate concentrations. Transcriptional regulation is one of the most important mechanisms in the response of plants to NH4+ toxicity, but the nature of the involvement of transcription factors (TFs) in this regulation remains unclear. Here, RNA‐seq analysis was performed on Arabidopsis roots to screen for ammonium‐responsive TFs. WRKY46, the member of the WRKY transcription factor family most responsive to NH4+, was selected. We defined the role of WRKY46 using mutation and overexpression assays, and characterized the regulation of NUDX9 and indole‐3‐acetic acid (IAA)‐conjugating genes by WRKY46 via yeast one‐hybrid and electrophoretic mobility shift assays and chromatin immunoprecipitation‐quantitative real‐time polymerase chain reaction (ChIP‐qPCR). Knockout of WRKY46 increased, while overexpression of WRKY46 decreased, NH4+‐suppression of the primary root. WRKY46 is shown to directly bind to the promoters of the NUDX9 and IAA‐conjugating genes (GH3.1, GH3.6, UGT75D1, UGT84B2) and to inhibit their transcription, thus positively regulating free IAA content and stabilizing protein N‐glycosylation, leading to an inhibition of NH4+ efflux in the root elongation zone (EZ). We identify TF involvement in the regulation of NH4+ efflux in the EZ, and show that WRKY46 inhibits NH4+ efflux by negative regulation of NUDX9 and IAA‐conjugating genes.

Initially discovered in yeast, mitochondrial retrograde signalling has long been recognised as an essential in the perception of stress by eukaryotes. However, how to maintain the optimal amplitude and duration of its activation under natural stress conditions remains elusive in plants.Here, we show that TaSRO1, a major contributor to the agronomic performance of bread wheat plants exposed to salinity stress, interacted with a transmembrane domain-containing NAC transcription factor TaSIP1, which could translocate from the endoplasmic reticulum (ER) into the nucleus and activate some mitochondrial dysfunction stimulon (MDS) genes. Overexpression of TaSIP1 and TaSIP1-ΔC (a form lacking the transmembrane domain) in wheat both compromised the plants' tolerance of salinity stress, highlighting the importance of precise regulation of this signal cascade during salinity stress.The interaction of TaSRO1/TaSIP1, in the cytoplasm, arrested more TaSIP1 on the membrane of ER, and in the nucleus, attenuated the trans-activation activity of TaSIP1, therefore reducing the TaSIP1-mediated activation of MDS genes. Moreover, the overexpression of TaSRO1 rescued the inferior phenotype induced by TaSIP1 overexpression.Our study provides an orchestrating mechanism executed by the TaSRO1-TaSIP1 module that balances the growth and stress response via fine tuning the level of mitochondria retrograde signalling.