Photorespiratory metabolism in the cyanobacterial model Synechocystis sp. strain PCC 6803: A systems biology approach

蓝藻模型集胞藻中的光呼吸代谢。

• 批准号: 221780128
• 负责人: Dr. Joachim Kopka
• 金额: --
• 依托单位: Max-Planck-Institut für molekulare Pflanzenphysiologie (MPI-MP)
• 依托单位国家: 德国
• 项目类别: Research Units
• 财政年份: 2012
• 资助国家: 德国
• 起止时间: 2011-12-31 至 2016-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/221780128?language=en
• 关键词: Photorespiratory; metabolism; cyanobacterial; model; Synechocystis

The inorganic carbon-concentrating mechanism enables cyanobacterial growth in low CO2/high O2 environments and was until recently thought sufficient to suppress the oxygenase reaction of cyanobacterial ribulose-1,5-bisphosphate-carboxylase/-oxygenase (Rubisco). However, photorespiratory metabolism and glycolate detoxification were shown to be essential for cyanobacteria and were both endosymbiontically conveyed into the plant kingdom. We recently established Synechocystis sp. PCC 6803 as a cyanobacterial model for systems analyses at the transcriptome, metabolome and fluxome levels under conditions enhancing photorespiration by low inorganic carbon (Ci) availability (LC), in contrast to high Ci availability (HC), a condition that largely suppresses photorespiratory responses. These tools, specifically the flux phenotyping, allowed the formal demonstration of photorespiration and a photorespiratory burst upon shift from HC to LC using a glycolate accumulating ΔglcD1 glycolate dehydrogenase mutant. The same experiments indicated that transfer to LC conditions activates additional/alternative CO2 assimilation likely via phosphoenolpyruvate (PEP)-carboxylase, a reaction that is also utilized by higher plants. Here we propose to study the interaction of photorespiration with central metabolism by 13C-flux probing of glycolate dehydrogenase deletion mutants in combination with gene deletions that interfere with the CCM and the carbon-fixing PEP carboxylase pathway. The study will reveal, if and how the two main carbon fixing pathways interact.

无机碳浓缩机制使蓝藻生长在低CO2/高O2环境，直到最近被认为足以抑制蓝藻核酮糖-1，5-二磷酸羧化酶/-加氧酶（Rubisco）的加氧酶反应。然而，光呼吸代谢和乙醇酸解毒被证明是必不可少的蓝藻和内共生传递到植物王国。我们最近建立了集胞藻属PCC 6803作为系统分析的蓝藻模型在转录组，代谢组和fluxome水平的条件下，增强光呼吸低无机碳（Ci）的可用性（LC），相反，高Ci可用性（HC），在很大程度上抑制光呼吸反应的条件。这些工具，特别是通量表型分析，允许使用乙醇酸积累Δ glcD 1乙醇酸脱氢酶突变体正式证明从HC转变为LC时的光呼吸和光呼吸爆发。同样的实验表明，转移到LC条件下激活额外的/替代的CO2同化可能通过磷酸烯醇丙酮酸（PEP）-羧化酶，反应，也利用高等植物。在这里，我们建议研究光呼吸与中央代谢的相互作用，通过13 C-通量探测乙醇酸脱氢酶缺失突变体与基因缺失相结合，干扰CCM和碳固定PEP羧化酶途径。这项研究将揭示这两种主要的碳固定途径是否以及如何相互作用。