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

Soil salinity presents a significant challenge to plant growth due to its impact on essential mineral nutrients, such as iron (Fe). While Fe deficiency often arises alongside salt stress in natural environments, the molecular mechanisms that link Fe homeostasis with salt tolerance have remained elusive. This study identifies the Fe deficiency response regulator bHLH121 as a crucial player in conferring salt tolerance in Arabidopsis.

Plants with a loss-of-function mutation in bHLH121 exhibit heightened sensitivity to salt stress, featuring severely reduced primary root growth and diminished seedling biomass. Analysis of gene expression and tissue staining reveals that bHLH121 is essential for maintaining a balance of reactive oxygen species (ROS) in root tips during salt stress exposure.

Further investigation reveals that CATALASE 2 (CAT2) serves as a direct target of bHLH121, and overexpressing CAT2 counteracts the salt hypersensitivity observed in bhlh121 mutants. Importantly, this bHLH121-CAT2 regulatory module functions independently of the established SOS pathway, as plants carrying both bhlh121 and sos2 mutations display additive salt sensitivity.

In conclusion, this research uncovers a novel regulatory mechanism where bHLH121 orchestrates root tip redox homeostasis via CAT2, thereby enhancing salt tolerance. This work establishes a clear mechanistic connection between the Fe regulatory network and plant resilience against abiotic stress factors.