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拟南芥突变体 air1 表明 SOS3 在盐胁迫下调控花色素苷。

The Arabidopsis thaliana mutant air1 implicates SOS3 in the regulation of anthocyanins under salt stress.

机构信息

Department of Agriculture, University of Naples "Federico II", Via Università 100, 80055, Portici, Italy.

出版信息

Plant Mol Biol. 2013 Nov;83(4-5):405-15. doi: 10.1007/s11103-013-0099-z. Epub 2013 Aug 8.

Abstract

The accumulation of anthocyanins in plants exposed to salt stress has been largely documented. However, the functional link and regulatory components underlying the biosynthesis of these molecules during exposure to stress are largely unknown. In a screen of second site suppressors of the salt overly sensitive3-1 (sos3-1) mutant, we isolated the anthocyanin-impaired-response-1 (air1) mutant. air1 is unable to accumulate anthocyanins under salt stress, a key phenotype of sos3-1 under high NaCl levels (120 mM). The air1 mutant showed a defect in anthocyanin production in response to salt stress but not to other stresses such as high light, low phosphorous, high temperature or drought stress. This specificity indicated that air1 mutation did not affect anthocyanin biosynthesis but rather its regulation in response to salt stress. Analysis of this mutant revealed a T-DNA insertion at the first exon of an Arabidopsis thaliana gene encoding for a basic region-leucine zipper transcription factor. air1 mutants displayed higher survival rates compared to wild-type in oxidative stress conditions, and presented an altered expression of anthocyanin biosynthetic genes such as F3H, F3'H and LDOX in salt stress conditions. The results presented here indicate that AIR1 is involved in the regulation of various steps of the flavonoid and anthocyanin accumulation pathways and is itself regulated by the salt-stress response signalling machinery. The discovery and characterization of AIR1 opens avenues to dissect the connections between abiotic stress and accumulation of antioxidants in the form of flavonoids and anthocyanins.

摘要

在暴露于盐胁迫的植物中,花色苷的积累已被大量记录。然而,在胁迫下这些分子生物合成的功能联系和调节成分在很大程度上是未知的。在盐过度敏感 3-1(sos3-1)突变体的二次位点抑制筛选中,我们分离到花色苷损伤反应 1(air1)突变体。air1 不能在盐胁迫下积累花色苷,这是 sos3-1 在高 NaCl 水平(120 mM)下的关键表型。air1 突变体在响应盐胁迫时表现出色素合成缺陷,但对其他胁迫如高光、低磷、高温或干旱胁迫没有反应。这种特异性表明 air1 突变不影响花色苷的生物合成,而是影响其对盐胁迫的调节。对该突变体的分析表明,T-DNA 插入到拟南芥基因的第一个外显子中,该基因编码一个碱性区-亮氨酸拉链转录因子。与野生型相比,air1 突变体在氧化应激条件下具有更高的存活率,并且在盐胁迫条件下表现出花色苷生物合成基因如 F3H、F3'H 和 LDOX 的表达改变。这里呈现的结果表明,AIR1 参与了类黄酮和花色苷积累途径的各种步骤的调节,并且自身受到盐胁迫反应信号机制的调节。AIR1 的发现和特征为剖析非生物胁迫与以类黄酮和花色苷形式积累抗氧化剂之间的联系开辟了途径。

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