Scholarlink

Key message <p>GABA enhanced Al tolerance in broad bean through reducing Al accumulation by fine-tuning transport genes, reinforcing transcriptional activation of lignin biosynthesis, and enhancing internal detoxification by reconfiguring (iso)flavonoid biosynthesis.</p> Abstract <p>Aluminum (Al) toxicity is recognized as the second largest abiotic factor that limits crop productivity worldwide. While γ-aminobutyric acid (GABA) is known to enhance plant stress tolerance, its role in Al resistance, particularly in legumes like broad bean (<i>Vicia faba</i> L.), remains poorly understood at the molecular level. This study integrated physiological and transcriptomic analyses to elucidate the mechanisms by which exogenous GABA alleviates Al toxicity in broad bean. Results showed that 1000&#xa0;μM GABA significantly mitigated Al-induced root growth inhibition. Crucially, GABA reduced root and shoot Al concentrations by 52.0% and 55.2%, respectively, which was linked to the upregulation of <i>VfALMT1</i> (mediating Al efflux) and downregulation of <i>VfNIP1;2</i> (mediating Al root-to-shoot translocation). Concurrently, GABA alleviated the Al-induced suppression of lignin biosynthesis, reinforcing the cell wall as a physical barrier. Furthermore, GABA synergistically amplified the flavonoid biosynthesis pathway and uniquely activated the Al-suppressed isoflavonoid biosynthesis pathway, enhancing antioxidant capacity and potentially internal detoxification. These findings demonstrate that GABA enhances Al tolerance not by simply reversing Al-induced changes but by actively reprogramming key processes, including Al transport, cell wall fortification, and secondary metabolism. This study provides novel insights into GABA’s multifaceted role as a signaling molecule in plant Al stress tolerance, offering potential strategies for improving crop resilience in acid soils.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

GABA enhances broad bean aluminum tolerance via reducing uptake and reinforcing lignin and (iso)flavonoid synthesis

  • 期刊论文

  • 发表日期：

    2026年1月10日

查看全文
  • Haisheng Tang,
  • Jingya Yang,
  • Na Hu,
  • Yanshuang Li,
  • Xumei Huang,
  • Jianchu Xu,
  • Yunju Li,
  • Xiong Li

摘要

Key message

GABA enhanced Al tolerance in broad bean through reducing Al accumulation by fine-tuning transport genes, reinforcing transcriptional activation of lignin biosynthesis, and enhancing internal detoxification by reconfiguring (iso)flavonoid biosynthesis.

Abstract

Aluminum (Al) toxicity is recognized as the second largest abiotic factor that limits crop productivity worldwide. While γ-aminobutyric acid (GABA) is known to enhance plant stress tolerance, its role in Al resistance, particularly in legumes like broad bean (Vicia faba L.), remains poorly understood at the molecular level. This study integrated physiological and transcriptomic analyses to elucidate the mechanisms by which exogenous GABA alleviates Al toxicity in broad bean. Results showed that 1000 μM GABA significantly mitigated Al-induced root growth inhibition. Crucially, GABA reduced root and shoot Al concentrations by 52.0% and 55.2%, respectively, which was linked to the upregulation of VfALMT1 (mediating Al efflux) and downregulation of VfNIP1;2 (mediating Al root-to-shoot translocation). Concurrently, GABA alleviated the Al-induced suppression of lignin biosynthesis, reinforcing the cell wall as a physical barrier. Furthermore, GABA synergistically amplified the flavonoid biosynthesis pathway and uniquely activated the Al-suppressed isoflavonoid biosynthesis pathway, enhancing antioxidant capacity and potentially internal detoxification. These findings demonstrate that GABA enhances Al tolerance not by simply reversing Al-induced changes but by actively reprogramming key processes, including Al transport, cell wall fortification, and secondary metabolism. This study provides novel insights into GABA’s multifaceted role as a signaling molecule in plant Al stress tolerance, offering potential strategies for improving crop resilience in acid soils.