首页> 美国卫生研究院文献>Journal of Bacteriology >Succinate Dehydrogenase and Other Respiratory Pathways in Thylakoid Membranes of Synechocystis sp. Strain PCC 6803: Capacity Comparisons and Physiological Function
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Succinate Dehydrogenase and Other Respiratory Pathways in Thylakoid Membranes of Synechocystis sp. Strain PCC 6803: Capacity Comparisons and Physiological Function

机译:突囊藻类囊体膜中的琥珀酸脱氢酶和其他呼吸途径。菌株PCC 6803:容量比较和生理功能

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摘要

Respiration in cyanobacterial thylakoid membranes is interwoven with photosynthetic processes. We have constructed a range of mutants that are impaired in several combinations of respiratory and photosynthetic electron transport complexes and have examined the relative effects on the redox state of the plastoquinone (PQ) pool by using a quinone electrode. Succinate dehydrogenase has a major effect on the PQ redox poise, as mutants lacking this enzyme showed a much more oxidized PQ pool. Mutants lacking type I and II NAD(P)H dehydrogenases also had more oxidized PQ pools. However, in the mutant lacking type I NADPH dehydrogenase, succinate was essentially absent and effective respiratory electron donation to the PQ pool could be established after addition of 1 mM succinate. Therefore, lack of the type I NADPH dehydrogenase had an indirect effect on the PQ pool redox state. The electron donation capacity of succinate dehydrogenase was found to be an order of magnitude larger than that of type I and II NAD(P)H dehydrogenases. The reason for the oxidized PQ pool upon inactivation of type II NADH dehydrogenase may be related to the facts that the NAD pool in the cell is much smaller than that of NADP and that the NAD pool is fully reduced in the mutant without type II NADH dehydrogenase, thus causing regulatory inhibition. The results indicate that succinate dehydrogenase is the main respiratory electron transfer pathway into the PQ pool and that type I and II NAD(P)H dehydrogenases regulate the reduction level of NADP and NAD, which, in turn, affects respiratory electron flow through succinate dehydrogenase.
机译:蓝藻类囊体膜的呼吸与光合作用交织在一起。我们已经构建了一系列突变体,这些突变体在呼吸和光合作用电子传输复合体的几种组合中受损,并且已经通过使用醌电极检查了对塑体醌(PQ)池氧化还原状态的相对影响。琥珀酸脱氢酶对PQ氧化还原平衡具有重大影响,因为缺乏这种酶的突变体显示出更多的氧化PQ库。缺乏I和II型NAD(P)H脱氢酶的突变体也具有更多的氧化PQ库。但是,在缺少I型NADPH脱氢酶的突变体中,琥珀酸基本上不存在,在加入1 mM琥珀酸后,可以将有效的呼吸电子捐赠给PQ库。因此,缺乏I型NADPH脱氢酶对PQ池氧化还原状态有间接影响。发现琥珀酸脱氢酶的电子给予能力比I和II型NAD(P)H脱氢酶大一个数量级。 II型NADH脱氢酶失活后PQ池被氧化的原因可能与以下事实有关:细胞中的NAD池比NADP小得多,并且在没有II型NADH脱氢酶的突变体中NAD池被完全还原,从而引起调节抑制。结果表明,琥珀酸脱氢酶是进入PQ池的主要呼吸电子转移途径,I型和II型NAD(P)H脱氢酶调节NADP和NAD的还原水平,进而影响通过琥珀酸脱氢酶的呼吸电子流。 。

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