Root Remodeling Mechanisms and Salt Tolerance Trade-Offs: The Roles of HKT1, TMAC2, and TIP2;2 in Arabidopsis

Abstract

Plant responses to salt stress involve complex processes integrating short- and long-term adaptations, including changes in ion transport, systemic signaling, root architecture, and biomass distribution. A key adaptive mechanism involves the regulation of sodium (Na+) and potassium (K+) ion transport via Class 1 HKT1 transporters, which reduce Na+ accumulation in shoots, thereby enhancing salinity tolerance but at the expense of lateral root development. In this study, we identified differential roles of TMAC2 in modulating ABA accumulation and lateral root development under salt stress in two distinct Arabidopsis genotypes, Col-0 and C24. Overexpression of TMAC2 in the Col-0 background increased ABA accumulation, resulting in reduced lateral root development, suggesting a positive feedback loop involving HKT1, TMAC2, and ABA signaling. In contrast, TMAC2 overexpression in C24 reduced ABA accumulation in lines overexpressing HKT1, indicating genotype-specific differences in the TMAC2-HKT1 interaction. Additionally, we observed that the co-expression of TMAC2 and HKT1 in Col-0 induced ABI4 and ABI5 transcription factors, which are known to mediate salt sensitivity. These findings reveal a regulatory network where TMAC2 and HKT1 modulate salt stress responses through genotype-dependent feedback mechanisms. Our results highlight the complexity of root remodeling under salt stress and the crucial role of genetic background in shaping these adaptive responses.