一种与原叶绿素酸酯氧化还原酶A的质体导入缺陷相关的植物卟啉症。
A plant porphyria related to defects in plastid import of protochlorophyllide oxidoreductase A.
作者信息
Pollmann Stephan, Springer Armin, Buhr Frank, Lahroussi Abder, Samol Iga, Bonneville Jean-Marc, Tichtinsky Gabrielle, von Wettstein Diter, Reinbothe Christiane, Reinbothe Steffen
机构信息
Université Joseph Fourier et Centre National de la Recherche Scientifique Unité Mixte de Recherche 5575, CERMO, BP53, Grenoble Cedex 9, France.
出版信息
Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):2019-23. doi: 10.1073/pnas.0610934104. Epub 2007 Jan 29.
Abstract
The plastid envelope of higher plant chloroplasts is a focal point of plant metabolism. It is involved in numerous pathways, including tetrapyrrole biosynthesis and protein translocation. Chloroplasts need to import a large number of proteins from the cytosol because most are encoded in the nucleus. Here we report that a loss-of-function mutation in the outer plastid envelope 16-kDa protein (oep16) gene causes a conditional seedling lethal phenotype related to defects in import and assembly of NADPH:protochlorophyllide (Pchlide) oxidoreductase A. In the isolated knockout mutant of Arabidopsis thaliana, excess Pchlide accumulated in the dark operated as photosensitizer and provoked cell death during greening. Our results highlight the essential role of the substrate-dependent plastid import pathway of precursor Pchlide oxidoreductase A for seedling survival and the avoidance of developmentally programmed porphyria in higher plants.
摘要
高等植物叶绿体的质体被膜是植物新陈代谢的一个焦点。它参与众多途径，包括四吡咯生物合成和蛋白质转运。由于大多数蛋白质是由细胞核编码的，叶绿体需要从细胞质中导入大量蛋白质。在这里我们报道，外质体被膜16 kDa蛋白（oep16）基因的功能缺失突变导致一种与NADPH：原叶绿素酸酯（Pchlide）氧化还原酶A的导入和组装缺陷相关的条件性幼苗致死表型。在拟南芥的分离敲除突变体中，过量的Pchlide在黑暗中积累，作为光敏剂并在绿化过程中引发细胞死亡。我们的结果突出了前体Pchlide氧化还原酶A的底物依赖性质体导入途径对高等植物幼苗存活和避免程序性卟啉症的重要作用。
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