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拟南芥 mtHSC70-1 在建立 COX 依赖的呼吸作用和氧化还原稳态中发挥重要作用。

Arabidopsis mtHSC70-1 plays important roles in the establishment of COX-dependent respiration and redox homeostasis.

机构信息

Hebei Key Laboratory of Molecular and Cellular Biology, Hebei Collaboration Innovation Center for Cell Signaling, Key Laboratory of Molecular and Cellular Biology of Ministry of Education, College of Life Science, Hebei Normal University, Shijiazhuang, China.

College of Biological Science and Engineering, Xingtai University, Xingtai, China.

出版信息

J Exp Bot. 2019 Oct 24;70(20):5575-5590. doi: 10.1093/jxb/erz357.

DOI:10.1093/jxb/erz357
PMID:31384929
Abstract

The 70 kDa heat shock proteins function as molecular chaperones and are involved in diverse cellular processes. However, the functions of the plant mitochondrial HSP70s (mtHSC70s) remain unclear. Severe growth defects were observed in the Arabidopsis thaliana mtHSC70-1 knockout lines, mthsc70-1a and mthsc70-1b. Conversely, the introduction of the mtHSC70-1 gene into the mthsc70-1a background fully reversed the phenotypes, indicating that mtHSC70-1 is essential for plant growth. The loss of mtHSC70-1 functions resulted in abnormal mitochondria and alterations to respiration because of an inhibition of the cytochrome c oxidase (COX) pathway and the activation of the alternative respiratory pathway. Defects in COX assembly were observed in the mtHSC70-1 knockout lines, leading to decreased COX activity. The mtHSC70-1 knockout plants have increased levels of reactive oxygen species (ROS). The introduction of the Mn-superoxide dismutase 1 (MSD1) or the catalase 1 (CAT1) gene into the mthsc70-1a plants decreased ROS levels, reduced the expression of alternative oxidase, and partially rescued growth. Taken together, our data suggest that mtHSC70-1 plays important roles in the establishment of COX-dependent respiration.

摘要

70kDa 热休克蛋白作为分子伴侣发挥功能,参与多种细胞过程。然而,植物线粒体 HSP70(mtHSC70)的功能尚不清楚。拟南芥 mtHSC70-1 敲除系 mthsc70-1a 和 mthsc70-1b 表现出严重的生长缺陷。相反,将 mtHSC70-1 基因导入 mthsc70-1a 背景中完全逆转了表型,表明 mtHSC70-1 对植物生长是必需的。mtHSC70-1 功能丧失导致线粒体异常和呼吸作用改变,这是由于细胞色素 c 氧化酶(COX)途径的抑制和替代呼吸途径的激活。在 mtHSC70-1 敲除系中观察到 COX 组装缺陷,导致 COX 活性降低。mtHSC70-1 敲除植物的活性氧(ROS)水平增加。将 Mn-超氧化物歧化酶 1(MSD1)或过氧化氢酶 1(CAT1)基因导入 mthsc70-1a 植物中,降低了 ROS 水平,降低了替代氧化酶的表达,并部分挽救了生长。总之,我们的数据表明 mtHSC70-1 在 COX 依赖性呼吸的建立中发挥重要作用。

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