The bHLH121-CAT2 module maintains root tip redox homeostasis to confer salt tolerance additively with the SOS pathway in Arabidopsis

Soil salinity inhibits plant growth, in part, by restricting the availability of essential mineral nutrients such as iron (Fe). Although Fe deficiency frequently coincides with salt stress in the field, the molecular mechanisms integrating Fe homeostasis with salt tolerance remain largely unknown. Here, we identify the Fe deficiency response regulator bHLH121 as a key coordinator of salt tolerance in Arabidopsis. Loss-of-function mutants of bHLH121 exhibit pronounced hypersensitivity to salt stress, with severely impaired primary root elongation and reduced seedling biomass. Transcriptomic and histochemical analyses reveal that bHLH121 is required to maintain reactive oxygen species (ROS) homeostasis specifically in root tips under salt stress. We further demonstrate that CATALASE 2 (CAT2) is a direct downstream target of bHLH121, and that CAT2 overexpression fully rescues the salt hypersensitivity of the bhlh121 mutant. Importantly, this bHLH121-CAT2 module operates independently of the classical SOS pathway, as sos2 bhlh121 double mutants display additive salt sensitivity. Together, our findings uncover a novel regulatory module in which bHLH121 governs root tip redox homeostasis through CAT2 to confer salt tolerance, providing a direct mechanistic link between the Fe regulatory network and abiotic stress resilience in plants.