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高等植物质体NAD(P)H脱氢酶样复合体(NDH)是一种高效质子泵,可通过循环电子流增加ATP生成。

The higher plant plastid NAD(P)H dehydrogenase-like complex (NDH) is a high efficiency proton pump that increases ATP production by cyclic electron flow.

作者信息

Strand Deserah D, Fisher Nicholas, Kramer David M

机构信息

MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48823.

MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48823; Department of Biochemistry and Molecular Biology, Michigan State University, East Lansing, Michigan 48823.

出版信息

J Biol Chem. 2017 Jul 14;292(28):11850-11860. doi: 10.1074/jbc.M116.770792. Epub 2017 May 30.

DOI:10.1074/jbc.M116.770792
PMID:28559282
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5512078/
Abstract

Cyclic electron flow around photosystem I (CEF) is critical for balancing the photosynthetic energy budget of the chloroplast by generating ATP without net production of NADPH. We demonstrate that the chloroplast NADPH dehydrogenase complex, a homolog to respiratory Complex I, pumps approximately two protons from the chloroplast stroma to the lumen per electron transferred from ferredoxin to plastoquinone, effectively increasing the efficiency of ATP production via CEF by 2-fold compared with CEF pathways involving non-proton-pumping plastoquinone reductases. By virtue of this proton-pumping stoichiometry, we hypothesize that NADPH dehydrogenase not only efficiently contributes to ATP production but operates near thermodynamic reversibility, with potentially important consequences for remediating mismatches in the thylakoid energy budget.

摘要

围绕光系统I的循环电子流(CEF)对于通过产生ATP而不净产生NADPH来平衡叶绿体的光合能量预算至关重要。我们证明,叶绿体NADPH脱氢酶复合体,一种与呼吸复合体I同源的物质,每将一个电子从铁氧化还原蛋白转移到质体醌,就会从叶绿体基质向类囊体腔泵出大约两个质子,与涉及非质子泵质体醌还原酶的CEF途径相比,有效地将通过CEF产生ATP的效率提高了2倍。基于这种质子泵化学计量,我们推测NADPH脱氢酶不仅有效地促进了ATP的产生,而且在接近热力学可逆性的条件下运行,这可能对修复类囊体能量预算中的不匹配具有重要意义。

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本文引用的文献

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Redox regulation of the antimycin A sensitive pathway of cyclic electron flow around photosystem I in higher plant thylakoids.高等植物类囊体中围绕光系统I的循环电子流的抗霉素A敏感途径的氧化还原调节。
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