ZmARR2 promotes salt tolerance in maize through a redox-related pathway

Soil salinization severely limits crop productivity by disrupting ionic and redox homeostasis. Cytokinin signaling mediated by type-B Arabidopsis response regulators (B-ARRs) has been implicated in stress acclimation in plants. However, the downstream transcriptional targets and regulatory networks governed by B-ARRs in maize ( Zea mays ) during the salinity-stress response have not been systematically elucidated. Here, we identified nine type-B ARR genes in the maize genome and determined that the expression of most of these genes responds to salt stress, with ZmARR2 showing the strongest induction. ZmARR2 encodes a transcription factor with transcriptional activation activity. Loss-of-function Zmarr2 mutants were more sensitive to salinity stress and exhibited more pronounced membrane damage than the wild type, whereas plants overexpressing ZmARR2 showed altered Na + contents and enhanced survival under salt stress. DNA affinity purification sequencing (DAP-seq) and RNA sequencing revealed ZmARR2 target genes that are involved in oxidoreductase activity, metal ion binding, and protein folding. Combined DAP-seq, differential gene expression analysis, and luciferase reporter assays showed that ZmARR2 positively regulates the expression of ZmRBOH4 , which encodes a respiratory burst oxidase homolog responsible for reactive oxygen species (ROS) production. ZmRBOH4 likely contributes to salt tolerance by modulating ROS-mediated signaling. These findings identify ZmARR2 as a regulator of ZmRBOH4 -dependent ROS signaling, providing molecular evidence for cytokinin-mediated salt tolerance in maize.