Root growth and architecture are markedly influenced by both developmental and environmental cues. Sugars integrate different stimuli and are essential building blocks and signaling molecules for modulating the root system. Members from the SUGAR WILL EVENTUALLY BE EXPORTED TRANSPORTER (SWEET) family facilitate the transport of different sugars over cellular membranes and steer both inter and intracellular distribution of sugars. SWEET17 represents a fructose-specific sugar porter localized to the vacuolar membrane, the tonoplast. Here, we analyzed how SWEET17-dependent fructose released from vacuoles affects root growth during drought stress in Arabidopsis (Arabidopsis thaliana). We found that the SWEET17 gene was predominantly expressed in the root vasculature and in meristematic cells of the root tip. SWEET17 expression appeared markedly induced during lateral root (LR) outgrowth and under drought. Moreover, fructose repressed primary root growth but induced density and length of first order LRs. Consistently, sweet17 knock-out mutants exhibited reduced LR growth and a diminished expression of LR-development-related transcription factors during drought stress, resulting in impaired drought tolerance of sweet17 mutants. We discuss how SWEET17 activity integrates drought-induced cellular responses into fructose signaling necessary for modulation of the root system and maximal drought tolerance.

中文翻译：

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液泡果糖转运蛋白 SWEET17 对根系发育和耐旱性至关重要

根系的生长和结构明显受到发育和环境因素的影响。糖整合了不同的刺激，是调节根系的重要组成部分和信号分子。SUGAR 的成员最终将成为出口转运蛋白 (SWEET) 家族的成员，促进不同糖在细胞膜上的转运，并控制糖在细胞间和细胞内的分布。SWEET17 代表一种定位于液泡膜液泡膜的果糖特异性糖转运体。在这里，我们分析了从液泡释放的 SWEET17 依赖性果糖如何影响拟南芥（Arabidopsis thaliana）干旱胁迫期间的根系生长。我们发现 SWEET17 基因主要在根脉管系统和根尖的分生细胞中表达。SWEET17 表达在侧根 (LR) 生长和干旱条件下出现显着诱导。此外，果糖抑制初生根生长，但诱导一级LRs的密度和长度。一致地，sweet17 敲除突变体在干旱胁迫期间表现出 LR 生长减少和 LR 发育相关转录因子表达减少，导致 sweet17 突变体的耐旱性受损。我们讨论了 SWEET17 活性如何将干旱诱导的细胞反应整合到调节根系和最大耐旱性所必需的果糖信号中。sweet17 敲除突变体在干旱胁迫期间表现出 LR 生长减少和 LR 发育相关转录因子表达减少，导致 sweet17 突变体的耐旱性受损。我们讨论了 SWEET17 活性如何将干旱诱导的细胞反应整合到调节根系和最大耐旱性所必需的果糖信号中。sweet17 敲除突变体在干旱胁迫期间表现出 LR 生长减少和 LR 发育相关转录因子表达减少，导致 sweet17 突变体的耐旱性受损。我们讨论了 SWEET17 活性如何将干旱诱导的细胞反应整合到调节根系和最大耐旱性所必需的果糖信号中。