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面包小麦中铝耐受性的内在和诱导代谢特征:一种比较代谢组学方法。

Intrinsic and induced metabolic signatures underpin aluminum tolerance in bread wheat: a comparative metabolomics approach.

作者信息

Çatav Şükrü Serter, Elgin Emine Sonay, Küçükakyüz Köksal, Dağ Çağdaş

机构信息

Department of Biology, Faculty of Science, Muğla Sıtkı Koçman University, Muğla, Turkey.

Department of Chemistry, Faculty of Science, Muğla Sıtkı Koçman University, Muğla, Turkey.

出版信息

Physiol Mol Biol Plants. 2025 Jun;31(6):1011-1026. doi: 10.1007/s12298-025-01622-1. Epub 2025 Jul 22.

DOI:10.1007/s12298-025-01622-1
PMID:40756439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12314282/
Abstract

UNLABELLED

Aluminum (Al) toxicity is a major impediment to plant growth and yield in low pH soils. Exclusion and/or vacuolar sequestration of Al with organic acids and phenolic compounds is the primary tolerance mechanism utilized by plants to mitigate Al toxicity. However, little is known about the intrinsic and Al-induced metabolic differences underlying intraspecific variability in tolerance to Al toxicity. To fill this gap, we determined root metabolic profiles of Al-sensitive (Golia-99) and Al-tolerant (Demir-2000) bread wheat cultivars treated with 0, 10, and 30 µM AlCl·6HO using nuclear magnetic resonance (NMR) spectroscopy. Our results showed that there were marked differences in the concentrations of numerous metabolites between Golia-99 and Demir-2000 roots under both control and Al stress conditions. In this regard, a number of metabolites from the amino acid and TCA groups, such as citrate, cysteine, glutamate, isocitrate, phenylalanine, and succinate, were found to be intrinsically higher levels in Demir-2000 than in Golia-99. In addition, Al toxicity led to the accumulation of asparagine, glutamine, putrescine, pyroglutamate, and soluble sugars in Demir-2000 roots. Furthermore, Al treatments significantly altered many metabolic pathways in both cultivar-specific and cultivar-independent manners. The major pathways contributing to the difference in Al toxicity tolerance between Demir-2000 and Golia-99 were arginine biosynthesis, glycolysis/gluconeogenesis, and the metabolisms of cysteine and methionine, glutathione, glycine, serine and threonine, pyruvate, sulfur, and tyrosine. Overall, our results suggest that the distinct patterns of Al-induced overrepresentation in amino acid, carbohydrate, and energy metabolism play an important role in explaining the differential tolerance capacities of Demir-2000 and Golia-99 to Al toxicity. The outcomes of this study may provide valuable insights into improving Al tolerance in wheat through breeding and genetic engineering.

SUPPLEMENTARY INFORMATION

The online version contains supplementary material available at 10.1007/s12298-025-01622-1.

摘要

未标注

铝(Al)毒性是低pH值土壤中植物生长和产量的主要障碍。植物利用有机酸和酚类化合物排除和/或将铝隔离在液泡中,这是其减轻铝毒性的主要耐受机制。然而,关于植物对铝毒性耐受性种内变异背后的内在和铝诱导的代谢差异知之甚少。为了填补这一空白,我们使用核磁共振(NMR)光谱法测定了用0、10和30 µM AlCl₃·6H₂O处理的铝敏感型(戈利亚-99)和铝耐受型(德米尔-2000)面包小麦品种的根系代谢谱。我们的结果表明,在对照和铝胁迫条件下,戈利亚-99和德米尔-2000根系中许多代谢物的浓度存在显著差异。在这方面,发现德米尔-2000中来自氨基酸和三羧酸(TCA)组的一些代谢物,如柠檬酸、半胱氨酸、谷氨酸、异柠檬酸、苯丙氨酸和琥珀酸,其内在水平高于戈利亚-99。此外,铝毒性导致德米尔-2000根系中天门冬酰胺、谷氨酰胺、腐胺、焦谷氨酸和可溶性糖的积累。此外,铝处理以品种特异性和品种非特异性方式显著改变了许多代谢途径。导致德米尔-2000和戈利亚-99对铝毒性耐受性差异的主要途径是精氨酸生物合成、糖酵解/糖异生以及半胱氨酸和蛋氨酸、谷胱甘肽、甘氨酸、丝氨酸和苏氨酸、丙酮酸、硫和酪氨酸的代谢。总体而言,我们的结果表明,铝诱导的氨基酸、碳水化合物和能量代谢中过度表达的独特模式在解释德米尔-2000和戈利亚-99对铝毒性的不同耐受能力方面起着重要作用。本研究结果可能为通过育种和基因工程提高小麦对铝的耐受性提供有价值的见解。

补充信息

在线版本包含可在10.1007/s12298-025-01622-1获取的补充材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/2b27e1c31072/12298_2025_1622_Fig9_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/2b27e1c31072/12298_2025_1622_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/9ea192fd72dc/12298_2025_1622_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/c976e54a5971/12298_2025_1622_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/e1115c8cdc1a/12298_2025_1622_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/9a5fd74b1a31/12298_2025_1622_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/d91c130c0ffa/12298_2025_1622_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/cfe4bcf8723b/12298_2025_1622_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/d6d182729da4/12298_2025_1622_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/7bd03b2c1e7a/12298_2025_1622_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7112/12314282/2b27e1c31072/12298_2025_1622_Fig9_HTML.jpg

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