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缺铁时针对特定 Fe 蛋白的铁代谢调控程序。

A Program for Iron Economy during Deficiency Targets Specific Fe Proteins.

机构信息

Biology Department, Colorado State University, Fort Collins, Colorado 80523-1878.

Department of Bioagricultural Sciences and Pest Management, Colorado State University, Fort Collins, Colorado 80523-1177.

出版信息

Plant Physiol. 2018 Jan;176(1):596-610. doi: 10.1104/pp.17.01497. Epub 2017 Nov 17.

DOI:10.1104/pp.17.01497
PMID:29150559
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5761800/
Abstract

Iron (Fe) is an essential element for plants, utilized in nearly every cellular process. Because the adjustment of uptake under Fe limitation cannot satisfy all demands, plants need to acclimate their physiology and biochemistry, especially in their chloroplasts, which have a high demand for Fe. To investigate if a program exists for the utilization of Fe under deficiency, we analyzed how hydroponically grown Arabidopsis () adjusts its physiology and Fe protein composition in vegetative photosynthetic tissue during Fe deficiency. Fe deficiency first affected photosynthetic electron transport with concomitant reductions in carbon assimilation and biomass production when effects on respiration were not yet significant. Photosynthetic electron transport function and protein levels of Fe-dependent enzymes were fully recovered upon Fe resupply, indicating that the Fe depletion stress did not cause irreversible secondary damage. At the protein level, ferredoxin, the cytochrome- complex, and Fe-containing enzymes of the plastid sulfur assimilation pathway were major targets of Fe deficiency, whereas other Fe-dependent functions were relatively less affected. In coordination, SufA and SufB, two proteins of the plastid Fe-sulfur cofactor assembly pathway, were also diminished early by Fe depletion. Iron depletion reduced mRNA levels for the majority of the affected proteins, indicating that loss of enzyme was not just due to lack of Fe cofactors. SufB and ferredoxin were early targets of transcript down-regulation. The data reveal a hierarchy for Fe utilization in photosynthetic tissue and indicate that a program is in place to acclimate to impending Fe deficiency.

摘要

铁(Fe)是植物必需的元素,参与几乎所有细胞过程。由于在 Fe 限制下吸收的调节不能满足所有需求,因此植物需要调节其生理学和生物化学特性,特别是在对 Fe 有高需求的叶绿体中。为了研究在缺乏 Fe 的情况下是否存在利用 Fe 的程序,我们分析了水培拟南芥()在 Fe 缺乏时如何在营养生长的光合组织中调节其生理学和 Fe 蛋白组成。Fe 缺乏首先影响光合电子传递,同时伴随着碳同化和生物量生产的减少,而对呼吸的影响尚不显著。当再次供应 Fe 时,光合电子传递功能和 Fe 依赖性酶的蛋白水平完全恢复,这表明 Fe 耗尽胁迫没有造成不可逆转的二次损伤。在蛋白质水平上,铁氧还蛋白、细胞色素复合体和质体硫同化途径中的 Fe 结合酶是 Fe 缺乏的主要靶标,而其他 Fe 依赖性功能受影响相对较小。协调地,质体 Fe-S 辅助因子组装途径中的 SufA 和 SufB 两种蛋白也因 Fe 缺乏而早期减少。Fe 耗竭降低了大多数受影响蛋白的 mRNA 水平,这表明酶的丧失不仅仅是由于缺乏 Fe 辅因子。SufB 和铁氧还蛋白是转录下调的早期靶标。这些数据揭示了光合组织中 Fe 利用的层次结构,并表明存在一个适应即将发生的 Fe 缺乏的程序。

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