Root remodeling mechanisms and salt tolerance trade-offs: The roles of HKT1, TMAC2, and TIP2;2 in Arabidopsis.

Plant responses to salt stress involve regulatory networks integrating ion transport, hormonal signaling, and root system architecture remodeling. A key adaptive mechanism is the regulation of sodium (Na⁺) transport by Class 1 HKT1 transporters, which compertamentalize Na⁺ in non-photosynthetic tissues. High HKT1 expression reduces Na+ accumulation in shoots, leading to increased salt tolerance, but simultaneously results in reduced lateral root development. In this study, we explored transcriptional responses that are altered by high HKT1 expression in root stelle in two Arabidopsis backgrounds, Col-0 and C24. We identified TMAC2, a negative ABA regulator, and TIP2:2, a tonoplast aquaporin, as key modulators of root development under salt stress. While TIP2:2 function was conserved, TMAC2 exhibited genotype-specific effects on ABA accumulation and HKT1-mediated salt sensitivity. Co-expression of TMAC2 and HKT1 in Col-0 upregulated ABI4 and ABI5, linking Na⁺ transport to ABA signaling. Our findings underscore genetic context in shaping salt responses and provide molecular targets for enhancing root plasticity under stress.