Relative expression of all mapped genes.

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、激素信号转导与根系结构重塑的调控网络。一类关键的适应机制是第1类HKT1转运蛋白（HKT1）对钠离子（Na⁺）转运的调控，该类蛋白可将Na⁺区室化至非光合组织中。HKT1的高表达会降低地上部分的Na+积累，从而提升植株的耐盐性，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）为材料，探究了根中柱内HKT1高表达所改变的转录响应。本研究鉴定出TMAC2（一种负调控脱落酸（ABA, abscisic acid）的因子）与TIP2:2（一种液泡膜水通道蛋白）作为盐胁迫下根系发育的关键调控因子。尽管TIP2:2的功能在不同遗传背景中保守，但TMAC2对ABA积累与HKT1介导的盐敏感性表现出基因型特异性的调控效应。在Col-0背景中共表达TMAC2与HKT1可上调ABI4与ABI5的表达，从而将Na+转运与ABA信号通路建立关联。本研究结果凸显了遗传背景在调控盐胁迫响应中的作用，并为提升胁迫下根系可塑性提供了分子靶点。