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硫氧还蛋白z和果糖激酶样蛋白1的氧化还原活性对于拟南芥的自养生长并非必需。

Redox activity of thioredoxin z and fructokinase-like protein 1 is dispensable for autotrophic growth of Arabidopsis thaliana.

作者信息

Wimmelbacher Matthias, Börnke Frederik

机构信息

Friedrich-Alexander-Universität, Department of Biology, Division of Biochemistry, Staudtstr. 5, 91058 Erlangen, Germany.

Leibniz-Institute of Vegetable and Ornamental Crops (IGZ), Theodor-Echtermeyer-Weg 1, 14979 Großbeeren, Germany Institute of Biochemistry and Biology, University of Potsdam, 14476 Potsdam, Germany

出版信息

J Exp Bot. 2014 Jun;65(9):2405-13. doi: 10.1093/jxb/eru122. Epub 2014 Mar 22.

Abstract

Redox modulation of protein activity by thioredoxins (TRXs) plays a key role in cellular regulation. Thioredoxin z (TRX z) and its interaction partner fructokinase-like protein 1 (FLN1) represent subunits of the plastid-encoded RNA polymerase (PEP), suggesting a role of both proteins in redox regulation of chloroplast gene expression. Loss of TRX z or FLN1 expression generates a PEP-deficient phenotype and renders the plants incapable to grow autotrophically. This study shows that PEP function in trx z and fln1 plants can be restored by complementation with redox-inactive TRX z C106S and FLN1 C105/106A protein variants, respectively. The complemented plants showed wild-type levels of chloroplast gene expression and were restored in photosynthetic capacity, indicating that redox regulation of PEP through TRX z/FLN1 per se is not essential for autotrophic growth. Promoter-reporter gene studies indicate that TRX z and FLN1 are expressed during early phases of leaf development while expression ceases at maturation. Taken together, our data support a model in which TRX z and FLN1 are essential structural components of the PEP complex and their redox activity might only play a role in the fine tuning of PEP function.

摘要

硫氧还蛋白(TRXs)对蛋白质活性的氧化还原调节在细胞调控中起着关键作用。硫氧还蛋白z(TRX z)及其相互作用伴侣果糖激酶样蛋白1(FLN1)是质体编码RNA聚合酶(PEP)的亚基,表明这两种蛋白在叶绿体基因表达的氧化还原调节中发挥作用。TRX z或FLN1表达缺失会产生PEP缺陷型表型,使植物无法自养生长。本研究表明,trx z和fln1植物中的PEP功能可分别通过用氧化还原无活性的TRX z C106S和FLN1 C105/106A蛋白变体进行互补来恢复。互补后的植物显示出野生型水平的叶绿体基因表达,光合能力也得以恢复,这表明通过TRX z/FLN1对PEP进行氧化还原调节本身对于自养生长并非必不可少。启动子-报告基因研究表明,TRX z和FLN1在叶片发育早期表达,而在成熟时表达停止。综上所述,我们的数据支持一个模型,即TRX z和FLN1是PEP复合物的重要结构成分,它们的氧化还原活性可能仅在PEP功能的微调中发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d51/4036507/0838e8006912/exbotj_eru122_f0001.jpg

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