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拟南芥中NADPH硫氧还蛋白还原酶C、2-半胱氨酸过氧化物酶和β型硫氧还蛋白在卡尔文-本森循环及苹果酸阀酶调控中的功能关系

The Functional Relationship between NADPH Thioredoxin Reductase C, 2-Cys Peroxiredoxins, and -Type Thioredoxins in the Regulation of Calvin-Benson Cycle and Malate-Valve Enzymes in Arabidopsis.

作者信息

Delgado-Requerey Víctor, Cejudo Francisco Javier, González María-Cruz

机构信息

Instituto de Bioquímica Vegetal y Fotosíntesis, Universidad de Sevilla and Consejo Superior de Investigaciones Científicas, Avenida Américo Vespucio 49, 41092 Sevilla, Spain.

Departamento de Bioquímica Vegetal y Biología Molecular, Facultad de Biología, Universidad de Sevilla, 41012 Sevilla, Spain.

出版信息

Antioxidants (Basel). 2023 May 3;12(5):1041. doi: 10.3390/antiox12051041.

DOI:10.3390/antiox12051041
PMID:37237907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10215429/
Abstract

The concerted regulation of chloroplast biosynthetic pathways and NADPH extrusion via malate valve depends on and thioredoxins (Trxs). The finding that decreased levels of the thiol-peroxidase 2-Cys peroxiredoxin (Prx) suppress the severe phenotype of Arabidopsis mutants lacking NADPH-dependent Trx reductase C (NTRC) and Trxs uncovered the central function of the NTRC-2-Cys-Prx redox system in chloroplast performance. These results suggest that Trxs are also regulated by this system; however, the functional relationship between NTRC, 2-Cys Prxs, and type Trxs is unknown. To address this issue, we generated mutants combining deficiencies in NTRC, 2-Cys Prx B, Trxs 1, and 4. The single and mutants showed a wild-type phenotype, growth retardation being noticed only in the double mutant. Moreover, the mutant displayed a more severe phenotype than the mutant, as shown by the impaired photosynthetic performance, altered chloroplast structure, and defective light-dependent reduction in the Calvin-Benson cycle and malate-valve enzymes. These effects were suppressed by the decreased contents of 2-Cys Prx, since the quadruple mutant displayed a wild-type-like phenotype. These results show that the activity of -type Trxs in the light-dependent regulation of biosynthetic enzymes and malate valve is controlled by the NTRC-2-Cys-Prx system.

摘要

叶绿体生物合成途径和通过苹果酸阀进行的NADPH外排的协同调节取决于硫氧还蛋白(Trxs)。硫醇过氧化物酶2-半胱氨酸过氧化物酶(Prx)水平降低可抑制缺乏NADPH依赖性硫氧还蛋白还原酶C(NTRC)和Trxs的拟南芥突变体的严重表型,这一发现揭示了NTRC-2-半胱氨酸-Prx氧化还原系统在叶绿体功能中的核心作用。这些结果表明Trxs也受该系统调节;然而,NTRC、2-半胱氨酸Prxs和Trxs类型之间的功能关系尚不清楚。为了解决这个问题,我们构建了NTRC、2-半胱氨酸Prx B、Trxs 1和4均有缺陷的突变体。单个和突变体表现出野生型表型,仅在双突变体中观察到生长迟缓。此外,突变体表现出比突变体更严重的表型,表现为光合性能受损、叶绿体结构改变以及卡尔文-本森循环和苹果酸阀酶的光依赖性还原缺陷。由于四重突变体表现出类似野生型的表型,这些效应被2-半胱氨酸Prx含量的降低所抑制。这些结果表明,Trxs类型在生物合成酶和苹果酸阀的光依赖性调节中的活性受NTRC-2-半胱氨酸-Prx系统控制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/45ed715d77c7/antioxidants-12-01041-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/f4936fe3863f/antioxidants-12-01041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/a8414f597c38/antioxidants-12-01041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/0092a59f0b05/antioxidants-12-01041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/9a90fde8452e/antioxidants-12-01041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/8ae70be577c8/antioxidants-12-01041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/111d51621c9c/antioxidants-12-01041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/9f5820dee049/antioxidants-12-01041-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/3cfb715c6a04/antioxidants-12-01041-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/781c75236fe4/antioxidants-12-01041-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/45ed715d77c7/antioxidants-12-01041-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/f4936fe3863f/antioxidants-12-01041-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/a8414f597c38/antioxidants-12-01041-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/0092a59f0b05/antioxidants-12-01041-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/9a90fde8452e/antioxidants-12-01041-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/8ae70be577c8/antioxidants-12-01041-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/111d51621c9c/antioxidants-12-01041-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/9f5820dee049/antioxidants-12-01041-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/3cfb715c6a04/antioxidants-12-01041-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/781c75236fe4/antioxidants-12-01041-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/24ca/10215429/45ed715d77c7/antioxidants-12-01041-g010.jpg

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