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促进γ-氨基丁酸积累以增强番茄的耐盐碱性。

Promoting γ-aminobutyric acid accumulation to enhances saline-alkali tolerance in tomato.

机构信息

College of Horticulture, Northwest A&F University, Yangling, Shaanxi 712100, P.R. China.

Key Laboratory of Protected Horticultural Engineering in Northwest, Ministry of Agriculture and Rural Affairs, Yangling, Shaanxi 712100, P.R. China.

出版信息

Plant Physiol. 2024 Nov 4;196(3):2089-2104. doi: 10.1093/plphys/kiae446.

DOI:10.1093/plphys/kiae446
PMID:39186533
Abstract

Saline-alkali stress is a widely distributed abiotic stress that severely limits plant growth. γ-Aminobutyric acid (GABA) accumulates rapidly in plants under saline-alkali stress, but the underlying molecular mechanisms and associated regulatory networks remain unclear. Here, we report a MYB-like protein, I-box binding factor (SlMYBI), which positively regulates saline-alkali tolerance through induced GABA accumulation by directly modulating the glutamate decarboxylase (GAD) gene SlGAD1 in tomato (Solanum lycopersicum L.). Overexpression of SlGAD1 increased GABA levels and decreased reactive oxygen species accumulation under saline-alkali stress, while silencing of SlGAD1 further suggested that SlGAD1 plays an active role in GABA synthesis and saline-alkali tolerance of tomato. In addition, we found that SlMYBI activates SlGAD1 transcription. Both overexpression of SlMYBI and editing of SlMYBI using CRISPR-Cas9 showed that SlMYBI regulates GABA synthesis by modulating SlGAD1 expression. Furthermore, the interaction of SlNF-YC1 with SlMYBI enhanced the transcriptional activity of SlMYBI on SlGAD1 to further improve saline-alkali tolerance in tomato. Interestingly, we found that ethylene signaling was involved in the GABA response to saline-alkali stress by RNA-seq analysis of SlGAD1-overexpressing lines. This study elucidates the involvement of SlMYBI in GABA synthesis regulation. Specifically, the SlMYBI-SlNF-YC1 module is involved in GABA accumulation in response to saline-alkali stress.

摘要

盐碱性胁迫是一种广泛分布的非生物胁迫,严重限制了植物的生长。在盐碱性胁迫下,植物中γ-氨基丁酸(GABA)迅速积累,但潜在的分子机制和相关的调控网络仍不清楚。在这里,我们报道了一个 MYB 样蛋白,I 框结合因子(SlMYBI),它通过直接调节谷氨酸脱羧酶(GAD)基因 SlGAD1 在番茄(Solanum lycopersicum L.)中正向调节盐碱性耐受性,从而诱导 GABA 积累。SlGAD1 的过表达增加了 GABA 水平,并在盐碱性胁迫下减少了活性氧的积累,而 SlGAD1 的沉默进一步表明 SlGAD1 在 GABA 合成和番茄的盐碱性耐受性中发挥着积极作用。此外,我们发现 SlMYBI 激活 SlGAD1 的转录。SlMYBI 的过表达和使用 CRISPR-Cas9 编辑 SlMYBI 都表明,SlMYBI 通过调节 SlGAD1 的表达来调节 GABA 的合成。此外,SlNF-YC1 与 SlMYBI 的相互作用增强了 SlMYBI 对 SlGAD1 的转录活性,从而进一步提高了番茄的耐盐碱性。有趣的是,我们通过 SlGAD1 过表达系的 RNA-seq 分析发现,乙烯信号参与了 GABA 对盐碱性胁迫的反应。本研究阐明了 SlMYBI 在 GABA 合成调控中的作用。具体来说,SlMYBI-SlNF-YC1 模块参与了 GABA 积累以应对盐碱性胁迫。

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