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铁氧还蛋白 5 缺失对藻类在不同硫饥饿阶段代谢的影响。

Ferredoxin5 Deletion Affects Metabolism of Algae during the Different Phases of Sulfur Deprivation.

机构信息

Biosciences Center, National Renewable Energy Laboratory, Golden, Colorado 80401

Biosciences Center, National Renewable Energy Laboratory, Golden, Colorado 80401.

出版信息

Plant Physiol. 2019 Oct;181(2):426-441. doi: 10.1104/pp.19.00457. Epub 2019 Jul 26.

Abstract

Ferredoxin5 (FDX5), a minor ferredoxin protein in the alga (), helps maintain thylakoid membrane integrity in the dark. Sulfur (S) deprivation has been used to achieve prolonged hydrogen production in green algae. Here, we propose that FDX5 is involved in algal responses to S-deprivation as well as to the dark. Specifically, we tested the role of FDX5 in both the initial aerobic and subsequent anaerobic phases of S-deprivation. Under S-deprived conditions, absence of FDX5 causes a distinct delay in achieving anoxia by affecting photosynthetic O evolution, accompanied by reduced acetate uptake, lower starch accumulation, and delayed/lower fermentative metabolite production, including photohydrogen. We attribute these differences to transcriptional and/or posttranslational regulation of acetyl-CoA synthetase and ADP-Glc pyrophosphorylase, and increased stability of the PSII D1 protein. Interestingly, increased levels of FDX2 and FDX1 were observed in the mutant under oxic, S-replete conditions, strengthening our previously proposed hypothesis that other ferredoxins compensate in response to a lack of FDX5. Taken together, the results of our omics and pull-down experiments confirmed biochemical and physiological results, suggesting that FDX5 may have other effects on metabolism through its interaction with multiple redox partners.

摘要

铁氧还蛋白 5(FDX5)是藻类中的一种次要铁氧还蛋白蛋白,有助于维持类囊体膜在黑暗中的完整性。硫(S)剥夺已被用于实现绿藻的长时间产氢。在这里,我们提出 FDX5 参与藻类对 S 剥夺以及黑暗的响应。具体来说,我们测试了 FDX5 在 S 剥夺的初始需氧和随后的厌氧阶段中的作用。在 S 剥夺条件下,FDX5 的缺失通过影响光合 O 释放而导致缺氧的出现明显延迟,伴随着乙酸盐摄取减少、淀粉积累减少以及发酵代谢物产生延迟/减少,包括光氢。我们将这些差异归因于乙酰辅酶 A 合成酶和 ADP-葡萄糖焦磷酸化酶的转录和/或翻译后调节,以及 PSII D1 蛋白稳定性的增加。有趣的是,在有氧、S 充足的条件下,突变体中观察到 FDX2 和 FDX1 的水平增加,这加强了我们之前提出的假设,即其他铁氧还蛋白在缺乏 FDX5 时会代偿。综上所述,我们的组学和下拉实验结果证实了生化和生理学结果,表明 FDX5 可能通过与多个氧化还原伴侣相互作用对代谢产生其他影响。

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