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醛脱氢酶在拟南芥吡啶核苷酸稳态中发挥作用。

Aldehyde Dehydrogenases Function in the Homeostasis of Pyridine Nucleotides in Arabidopsis thaliana.

作者信息

Missihoun Tagnon D, Kotchoni Simeon O, Bartels Dorothea

机构信息

Institute of Molecular Physiology and Biotechnology of Plants (IMBIO), University of Bonn, 53115, Bonn, Germany.

Department of Microbiology and Plant Pathology, University of California Riverside, Riverside, CA, 92521, USA.

出版信息

Sci Rep. 2018 Feb 13;8(1):2936. doi: 10.1038/s41598-018-21202-6.

DOI:10.1038/s41598-018-21202-6
PMID:29440669
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5811564/
Abstract

Aldehyde dehydrogenase enzymes (ALDHs) catalyze the oxidation of aliphatic and aromatic aldehydes to their corresponding carboxylic acids using NAD or NADP as cofactors and generating NADH or NADPH. Previous studies mainly focused on the ALDH role in detoxifying toxic aldehydes but their effect on the cellular NAD(P)H contents has so far been overlooked. Here, we investigated whether the ALDHs influence the cellular redox homeostasis. We used a double T-DNA insertion mutant that is defective in representative members of Arabidopsis thaliana ALDH families 3 (ALDH3I1) and 7 (ALDH7B4), and we examined the pyridine nucleotide pools, glutathione content, and the photosynthetic capacity of the aldh mutants in comparison with the wild type. The loss of function of ALDH3I1 and ALDH7B4 led to a decrease of NAD(P)H, NAD(P)H/NAD(P) ratio, and an alteration of the glutathione pools. The aldh double mutant had higher glucose-6-phosphate dehydrogenase activity than the wild type, indicating a high demand for reduced pyridine nucleotides. Moreover, the mutant had a reduced quantum yield of photosystem II and photosynthetic capacity at relatively high light intensities compared to the wild type. Altogether, our data revealed a role of ALDHs as major contributors to the homeostasis of pyridine nucleotides in plants.

摘要

醛脱氢酶(ALDHs)以NAD或NADP为辅因子,催化脂肪族和芳香族醛氧化为相应的羧酸,并生成NADH或NADPH。以往的研究主要集中在ALDH在解毒有毒醛类中的作用,但它们对细胞NAD(P)H含量的影响至今仍被忽视。在此,我们研究了ALDHs是否影响细胞氧化还原稳态。我们使用了一个双T-DNA插入突变体,该突变体在拟南芥ALDH家族3(ALDH3I1)和7(ALDH7B4)的代表性成员中存在缺陷,并且我们与野生型相比,检测了aldh突变体的吡啶核苷酸库、谷胱甘肽含量和光合能力。ALDH3I1和ALDH7B4功能的丧失导致NAD(P)H、NAD(P)H/NAD(P)比率降低,以及谷胱甘肽库的改变。aldh双突变体的葡萄糖-6-磷酸脱氢酶活性高于野生型,表明对还原型吡啶核苷酸有较高需求。此外,与野生型相比,该突变体在相对较高光照强度下光系统II的量子产率和光合能力降低。总之,我们的数据揭示了ALDHs在植物吡啶核苷酸稳态中作为主要贡献者的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/929901d310ea/41598_2018_21202_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/e351354aeda3/41598_2018_21202_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/8afced062534/41598_2018_21202_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/929901d310ea/41598_2018_21202_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/e351354aeda3/41598_2018_21202_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/8afced062534/41598_2018_21202_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/57c3/5811564/929901d310ea/41598_2018_21202_Fig3_HTML.jpg

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