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拟南芥中噻唑烷-4-羧酸(T4C)引发的耐盐性的转录机制。

Transcriptional mechanisms underlying thiazolidine-4-carboxylic acid (T4C)-primed salt tolerance in Arabidopsis.

作者信息

Hsu Wei-Yung, Wu Yi-Zhen, Lin Yu-Min, Zheng Mei-Juan, Chen Liang-Jwu, Yeh Chuan-Ming

机构信息

Institute of Molecular Biology, National Chung Hsing University, Taichung, Taiwan.

Advanced Plant and Food Crop Biotechnology Center, National Chung Hsing University, Taichung, Taiwan.

出版信息

Plant Cell Rep. 2025 Apr 28;44(5):104. doi: 10.1007/s00299-025-03486-x.

Abstract

T4C enhances salt stress tolerance in Arabidopsis by regulating osmotic and oxidative stress responses, activating ABA-related pathways, and inducing stress-responsive genes, including LEA proteins. High soil salinity is a major environmental stress that restricts crop productivity worldwide, necessitating strategies to enhance plant salt tolerance. Thiazolidine-4-carboxylic acid (T4C) has been reported to regulate proline biosynthesis, which is essential for abiotic stress responses, yet its role in stress tolerance remains unclear. This study investigates the physiological and molecular effects of T4C on Arabidopsis thaliana under salt stress conditions. T4C treatment alleviated salt-induced growth inhibition, improving biomass, relative water content, and chlorophyll retention while reducing oxidative stress markers such as malondialdehyde and anthocyanin accumulation. Transcriptomic and quantitative PCR analyses revealed that T4C upregulated proline biosynthesis genes, ABA-dependent signaling (RD29b, ABI3), and Late Embryogenesis Abundant (LEA) genes. Gene Ontology (GO) enrichment analysis identified biological processes related to water deprivation, ABA signaling, and salt stress, while Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated the involvement of phenylpropanoid biosynthesis, plant hormone signal transduction, and MAPK signaling in T4C-mediated responses. Notably, several transcription factors, including NAC, MYB, and WRKY family members, were identified as candidates involved in T4C-mediated stress priming. Collectively, these findings suggest that T4C may enhance salt tolerance by modulating osmotic balance, reducing oxidative stress, and activating stress-responsive genes and transcriptional regulators. Our results provide novel insights into the molecular mechanisms underlying T4C-mediated stress responses, highlighting its potential as a chemical priming agent to improve plant resilience under saline conditions.

摘要

T4C通过调节渗透和氧化应激反应、激活ABA相关途径以及诱导包括LEA蛋白在内的应激反应基因,增强拟南芥对盐胁迫的耐受性。高土壤盐度是限制全球作物生产力的主要环境胁迫,因此需要采取策略来提高植物的耐盐性。据报道,噻唑烷-4-羧酸(T4C)可调节脯氨酸的生物合成,脯氨酸对非生物胁迫反应至关重要,但其在胁迫耐受性中的作用仍不清楚。本研究调查了盐胁迫条件下T4C对拟南芥的生理和分子影响。T4C处理减轻了盐诱导的生长抑制,提高了生物量、相对含水量和叶绿素保留率,同时降低了丙二醛和花青素积累等氧化应激标志物。转录组学和定量PCR分析表明,T4C上调了脯氨酸生物合成基因、ABA依赖信号(RD29b、ABI3)和晚期胚胎发生丰富(LEA)基因。基因本体(GO)富集分析确定了与缺水、ABA信号和盐胁迫相关的生物学过程,而京都基因与基因组百科全书(KEGG)途径分析表明,苯丙烷生物合成、植物激素信号转导和MAPK信号参与了T4C介导的反应。值得注意的是,包括NAC、MYB和WRKY家族成员在内的几个转录因子被确定为参与T4C介导的胁迫引发的候选因子。总的来说,这些发现表明,T4C可能通过调节渗透平衡、降低氧化应激以及激活应激反应基因和转录调节因子来增强耐盐性。我们的结果为T4C介导的应激反应的分子机制提供了新的见解,突出了其作为一种化学引发剂在提高盐胁迫条件下植物恢复力方面的潜力。

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