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聚球藻UTEX 625气生细胞中HCO₃⁻和CO₂运输的能量来源。

Energy sources for HCO3- and CO2 transport in air-grown cells of synechococcus UTEX 625.

作者信息

Li Q, Canvin DT

机构信息

Department of Biology, Queen's University, Kingston, Ontario, Canada K7L 3N6.

出版信息

Plant Physiol. 1998 Mar;116(3):1125-32. doi: 10.1104/pp.116.3.1125.

DOI:10.1104/pp.116.3.1125
PMID:9501145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC35082/
Abstract

Light-dependent inorganic C (Ci) transport and accumulation in air-grown cells of Synechococcus UTEX 625 were examined with a mass spectrometer in the presence of inhibitors or artificial electron acceptors of photosynthesis in an attempt to drive CO2 or HCO3- uptake separately by the cyclic or linear electron transport chains. In the presence of 3-(3,4-dichlorophenyl)-1,1-dimethylurea, the cells were able to accumulate an intracellular Ci pool of 20 mm, even though CO2 fixation was completely inhibited, indicating that cyclic electron flow was involved in the Ci-concentrating mechanism. When 200 m N,N-dimethyl-p-nitrosoaniline was used to drain electrons from ferredoxin, a similar Ci accumulation was observed, suggesting that linear electron flow could support the transport of Ci. When carbonic anhydrase was not present, initial CO2 uptake was greatly reduced and the extracellular [CO2] eventually increased to a level higher than equilibrium, strongly suggesting that CO2 transport was inhibited and that Ci accumulation was the result of active HCO3- transport. With 3-(3,4-dichlorophenyl)-1, 1-dimethylurea-treated cells, Ci transport and accumulation were inhibited by inhibitors of CO2 transport, such as COS and Na2S, whereas Li+, an HCO3--transport inhibitor, had little effect. In the presence of N,N-dimethyl-p-nitrosoaniline, Ci transport and accumulation were not inhibited by COS and Na2S but were inhibited by Li+. These results suggest that CO2 transport is supported by cyclic electron transport and that HCO3- transport is supported by linear electron transport.

摘要

利用质谱仪,在光合作用抑制剂或人工电子受体存在的情况下,对集胞藻UTEX 625气生细胞中光依赖型无机碳(Ci)的转运和积累进行了研究,试图通过循环或线性电子传递链分别驱动二氧化碳或碳酸氢根的吸收。在3-(3,4-二氯苯基)-1,1-二甲基脲存在的情况下,尽管二氧化碳固定完全受到抑制,但细胞仍能够积累20 mM的细胞内Ci库,这表明循环电子流参与了Ci浓缩机制。当使用200 mM N,N-二甲基对亚硝基苯胺从铁氧化还原蛋白中排出电子时,观察到了类似的Ci积累,这表明线性电子流可以支持Ci的转运。当不存在碳酸酐酶时,初始二氧化碳吸收量大幅降低,细胞外[二氧化碳]最终升高至高于平衡的水平,这强烈表明二氧化碳转运受到抑制,且Ci积累是主动转运碳酸氢根的结果。对于用3-(3,4-二氯苯基)-1,1-二甲基脲处理的细胞,Ci的转运和积累受到二氧化碳转运抑制剂如COS和Na2S的抑制,而碳酸氢根转运抑制剂Li+的影响很小。在N,N-二甲基对亚硝基苯胺存在的情况下,Ci的转运和积累不受COS和Na2S的抑制,但受Li+的抑制。这些结果表明,二氧化碳转运由循环电子传递支持,而碳酸氢根转运由线性电子传递支持。

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