Regulation of iron-homeostasis in the chloroplast of Chlamydomonas reinhardtii: Dynamic remodeling of the photosynthetic machinery in response to iron availability

莱茵衣藻叶绿体中铁稳态的调节：响应铁可用性的光合机制的动态重塑

• 批准号: 29200592
• 负责人: Professor Dr. Michael Hippler
• 金额: --
• 依托单位: Arbeitsgruppe Plant Biochemistry and Biotechnology
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2006
• 资助国家: 德国
• 起止时间: 2005-12-31 至 2011-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/29200592?language=en
• 关键词: Regulation; iron; homeostasis; chloroplast; Chlamydomonas

Iron-deficiency is a serious nutritional problem for nearly all forms of life because the limited bioavailability of iron despite its natural abundance. The bioenergetic membranes of respiration and photosynthesis are a major cellular sink for iron because of the abundance of heme and iron-sulfur proteins in these pathways. A question addressed in this project is how redox energy metabolism is modified in response to various degrees of iron-deficiency. It is proposed to use the photosynthetic apparatus of the green alga Chlamydomonas reinhardtii as the experimental model because we can apply reverse genetics and whole systems approaches like proteomics to this problem. The proposal is designed to test the following hypothesis: There is a regulatory network that induces specific responses before an iron-deficiency dependent chlorotic phenotype becomes evident. This network senses the cellular or sub-cellular iron content and controls protein expression levels to regulate various processes including iron homeostasis and the remodeling process of the photosynthetic machinery. We will elucidate regulatory networks that operate in chloroplast iron-homeostasis with a focus on mechanisms that modulate bioenergetic pathways in the plastids in response to iron-deficiency and in particular on mechanisms that control and establish remodeling of photosystem I (PSI) and its light-harvesting proteins (LHCI).

缺铁是一个严重的营养问题，几乎所有形式的生命，因为有限的生物利用度的铁，尽管其天然丰富。呼吸和光合作用的生物能膜是铁的主要细胞库，因为在这些途径中富含血红素和铁硫蛋白。在这个项目中解决的一个问题是氧化还原能量代谢是如何修改，以应对不同程度的缺铁。建议使用绿色衣藻的光合机构作为实验模型，因为我们可以应用反向遗传学和整个系统的方法，如蛋白质组学的问题。该提案旨在测试以下假设：有一个监管网络，诱导特定的反应之前，缺铁依赖褪绿表型变得明显。该网络感测细胞或亚细胞铁含量并控制蛋白质表达水平以调节各种过程，包括铁稳态和光合机制的重塑过程。我们将阐明在叶绿体铁稳态中运作的调控网络，重点是调节质体中生物能途径的机制，以应对缺铁，特别是控制和建立光系统I（PSI）及其捕光蛋白（LHCI）的重塑机制。