List of primers used for expression.

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.

植物对盐胁迫的响应涉及整合离子转运、激素信号传导与根系结构重塑的调控网络。其中关键适应机制之一为1类HKT1转运蛋白（Class 1 HKT1 transporter）对钠离子（Na⁺）转运的调控，该蛋白可将Na⁺区隔化至非光合组织中。高表达HKT1可降低地上部分的Na⁺积累，从而提升植株耐盐性，但同时会抑制侧根发育。本研究以两种拟南芥遗传背景Col-0与C24的根中柱为材料，探究了高表达HKT1所引发的转录组变化。我们鉴定出两个盐胁迫下根系发育的关键调控因子：脱落酸（abscisic acid, ABA）负调控因子TMAC2，以及液泡膜水通道蛋白TIP2:2。尽管TIP2:2的功能在不同遗传背景中保守，TMAC2却对ABA积累及HKT1介导的盐敏感性表现出基因型特异性调控效应。在Col-0背景中共表达TMAC2与HKT1可上调ABA不敏感4（ABI4）与ABA不敏感5（ABI5）的表达，将Na⁺转运与ABA信号通路建立了功能关联。本研究结果凸显了遗传背景在塑造盐胁迫响应中的重要作用，并为胁迫环境下根系可塑性的遗传改良提供了分子靶标。