选择性氧化酶
生物
拟南芥
生物化学
代谢途径
替代补体途径
活性氧
基因表达
基因
细胞生物学
遗传学
植物
补体系统
突变体
抗体
作者
Е. В. Гармаш,Ilya O. Velegzhaninov,K.V. Ermolina,Anna V. Rybak,Р. В. Малышев
出处
期刊:Plant Science
[Elsevier]
日期:2019-11-06
卷期号:291: 110332-110332
被引量:33
标识
DOI:10.1016/j.plantsci.2019.110332
摘要
UV-B is a damaging component of solar radiation that inevitably reaches the Earth's surface. Plants have developed response mechanisms to adapt to UVB exposure. The alternative oxidase (AOX) catalyzes the ATP-uncoupling cyanide-resistant alternative pathway (AP) in plant mitochondria and is thought to be an important part of the cellular defense network under stress conditions. This study aimed to unravel the poorly understood functional significance of AOX1a induction in Arabidopsis thaliana leaves exposed to ecologically relevant doses of UVB radiation, by comparing wild-type (WT) plants with plants with modified expression of the AOX1a gene, either downregulated by antisense (AS-12) or overexpressed (XX-2). UVB exposure resulted in a phenotypic difference between lines. AOX1a overexpression resulted in the highest induction of AOX1A synthesis and MnSOD activity, and the lowest ROS level without pronounced changes in the phenotype relative to other genotypes. In AS-12 plants, expression of the majority of the genes encoding AOX was detected, other non-phosphorylating pathway components and antioxidant enzymes increased along with anthocyanin accumulation in leaves, and the ROS content was lower than in the WT. In addition to the expected AOX1 protein size (34 kDa), an AOX1 30 kDa band appeared under UVB exposure in all genotypes. However, in AS-12, the alterations in the transcript level and in the abundance of AOX1 protein isoforms induced by UVB could not fully functionally compensate for the lack of AOX1A. This was confirmed by the observed low AP capacity and increased levels of the oxidized form of ascorbate. These results highlight the importance of AOX in plant response to UVB for the control of a balanced metabolism, and indicate that AOX1a plays a key role in the regulation of the stress response.
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