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叶绿体2-半胱氨酸过氧化物酶在光合作用中的保护功能。来自转基因拟南芥的证据。

Protective function of chloroplast 2-cysteine peroxiredoxin in photosynthesis. Evidence from transgenic Arabidopsis.

作者信息

Baier M, Dietz K J

机构信息

Stoffwechselphysiologie und Biochemie der Pflanzen, Universität Bielefeld, Universitätsstrasse 25, 33615 Bielefeld, Germany.

出版信息

Plant Physiol. 1999 Apr;119(4):1407-14. doi: 10.1104/pp.119.4.1407.

DOI:10.1104/pp.119.4.1407
PMID:10198100
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC32026/
Abstract

2-Cysteine peroxiredoxins (2-CPs) constitute a ubiquitous group of peroxidases that reduce cell-toxic alkyl hydroperoxides to their corresponding alcohols. Recently, we cloned 2-CP cDNAs from plants and characterized them as chloroplast proteins. To elucidate the physiological function of the 2-CP in plant metabolism, we generated antisense mutants in Arabidopsis. In the mutant lines a 2-CP deficiency developed during early leaf and plant development and eventually the protein accumulated to wild-type levels. In young mutants with reduced amounts of 2-CP, photosynthesis was impaired and the levels of D1 protein, the light-harvesting protein complex associated with photosystem II, chloroplast ATP synthase, and ribulose-1,5-bisphosphate carboxylase/oxygenase were decreased. Photoinhibition was particularly pronounced after the application of the protein synthesis inhibitor, lincomycin. We concluded that the photosynthetic machinery needs high levels of 2-CP during leaf development to protect it from oxidative damage and that the damage is reduced by the accumulation of 2-CP protein, by the de novo synthesis and replacement of damaged proteins, and by the induction of other antioxidant defenses in 2-CP mutants.

摘要

2-半胱氨酸过氧化物酶(2-CPs)构成了一类普遍存在的过氧化物酶,可将细胞毒性的烷基过氧化氢还原为相应的醇类。最近,我们从植物中克隆了2-CP的cDNA,并将其鉴定为叶绿体蛋白。为了阐明2-CP在植物代谢中的生理功能,我们在拟南芥中构建了反义突变体。在突变株系中,2-CP缺乏在叶片和植株发育早期出现,最终该蛋白积累至野生型水平。在2-CP含量降低的年轻突变体中,光合作用受到损害,与光系统II相关的捕光蛋白复合体、叶绿体ATP合酶以及核酮糖-1,5-二磷酸羧化酶/加氧酶的水平均下降。在施用蛋白质合成抑制剂林可霉素后,光抑制现象尤为明显。我们得出结论,在叶片发育过程中,光合机构需要高水平的2-CP来保护其免受氧化损伤,并且在2-CP突变体中,2-CP蛋白的积累、受损蛋白的从头合成与替换以及其他抗氧化防御机制的诱导可减轻这种损伤。

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