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蓝细菌中二氧化碳的被动进入及其在细胞内依赖能量转化为碳酸氢根离子的过程由光系统I产生的质子动力势驱动。

Passive entry of CO2 and its energy-dependent intracellular conversion to HCO3- in cyanobacteria are driven by a photosystem I-generated deltamuH+.

作者信息

Tchernov D, Helman Y, Keren N, Luz B, Ohad I, Reinhold L, Ogawa T, Kaplan A

机构信息

Faculty of Science and Mathematics and The Minerva Center for Photosynthesis under Stress, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.

出版信息

J Biol Chem. 2001 Jun 29;276(26):23450-5. doi: 10.1074/jbc.M101973200. Epub 2001 Apr 10.

Abstract

CO(2) entry into Synechococcus sp. PCC7942 cells was drastically inhibited by the water channel blocker p-chloromercuriphenylsulfonic acid suggesting that CO(2) uptake is, for the most part, passive via aquaporins with subsequent energy-dependent conversion to HCO3(-). Dependence of CO(2) uptake on photosynthetic electron transport via photosystem I (PSI) was confirmed by experiments with electron transport inhibitors, electron donors and acceptors, and a mutant lacking PSI activity. CO(2) uptake was drastically inhibited by the uncouplers carbonyl cyanide m-chlorophenylhydrazone (CCCP) and ammonia but substantially less so by the inhibitors of ATP formation arsenate and N, N,-dicyclohexylcarbodiimide (DCCD). Thus a DeltamuH(+) generated by photosynthetic PSI electron transport apparently serves as the direct source of energy for CO(2) uptake. Under low light intensity, the rate of CO(2) uptake by a high-CO(2)-requiring mutant of Synechococcus sp. PCC7942, at a CO(2) concentration below its threshold for CO(2) fixation, was higher than that of the wild type. At saturating light intensity, net CO(2) uptake was similar in the wild type and in the mutant IL-3 suggesting common limitation by the rate of conversion of CO(2) to HCO3(-). These findings are consistent with a model postulating that electron transport-dependent formation of alkaline domains on the thylakoid membrane energizes intracellular conversion of CO(2) to HCO3(-).

摘要

水通道阻滞剂对氯汞苯磺酸可显著抑制二氧化碳进入聚球藻属PCC7942细胞,这表明大部分二氧化碳是通过水通道蛋白被动摄取的,随后通过能量依赖过程转化为碳酸氢根。通过使用电子传递抑制剂、电子供体和受体以及缺乏光系统I(PSI)活性的突变体进行实验,证实了二氧化碳摄取对通过光系统I的光合电子传递的依赖性。解偶联剂羰基氰化物间氯苯腙(CCCP)和氨可显著抑制二氧化碳摄取,但ATP形成抑制剂砷酸盐和N,N-二环己基碳二亚胺(DCCD)的抑制作用则小得多。因此,光合PSI电子传递产生的质子动力势显然是二氧化碳摄取的直接能量来源。在低光强度下,聚球藻属PCC7942的高二氧化碳需求突变体在低于其二氧化碳固定阈值的二氧化碳浓度下的二氧化碳摄取速率高于野生型。在饱和光强度下,野生型和突变体IL-3中的净二氧化碳摄取相似,这表明二氧化碳向碳酸氢根转化的速率存在共同限制。这些发现与一个模型一致,该模型假设类囊体膜上电子传递依赖的碱性结构域的形成会为细胞内二氧化碳向碳酸氢根的转化提供能量。

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