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雷帕霉素靶蛋白激酶(TOR激酶)对光合作用和线粒体呼吸的相互调节作用于…… (原文句子不完整,翻译可能存在一定局限性)

Reciprocal regulation of photosynthesis and mitochondrial respiration by TOR kinase in .

作者信息

Upadhyaya Shivani, Rao Basuthkar Jagadeeshwar

机构信息

Department of Biological Sciences Tata Institute of Fundamental Research (TIFR) Mumbai India.

Indian Institute of Science Education and Research (IISER) Tirupati Transit Campus: Sree Rama Engineering College Tirupati India.

出版信息

Plant Direct. 2019 Nov 14;3(11):e00184. doi: 10.1002/pld3.184. eCollection 2019 Nov.

Abstract

While the role of TOR kinase in the chloroplast biogenesis and transcriptional regulation of photosynthesis is well documented in , the functional relevance of this metabolic sensor kinase in chloroplast-mitochondria cross talk is unknown. Using as the model system, we demonstrate the role of TOR kinase in the regulation of chloroplast and mitochondrial functions: We show that TOR kinase inhibition impairs the maintenance of high ETR associated with PSII and low NPQ and inhibits efficient state transitions between PSII and PSI. While compromised photosynthetic functions are observed in TOR kinase inhibited cells, same conditions lead to augmentation in mitochondrial basal respiration rate by twofold and concomitantly a rise in ATP production. Interestingly, such upregulated mitochondrial functions in TOR-inhibited cells are mediated by fragmented mitochondria via upregulating COXIIb and downregulating Hxk1 and AOX1 protein levels. We propose that TOR kinase may act as a sensor that counter-regulates chloroplast versus mitochondrial functions in a normal cell.

摘要

虽然TOR激酶在叶绿体生物发生和光合作用转录调控中的作用在[具体文献]中有充分记载,但这种代谢传感激酶在叶绿体-线粒体相互作用中的功能相关性尚不清楚。以[具体模型系统]为模型,我们证明了TOR激酶在叶绿体和线粒体功能调控中的作用:我们发现,抑制TOR激酶会损害与光系统II相关的高电子传递速率(ETR)的维持以及低非光化学猝灭(NPQ),并抑制光系统II和光系统I之间的高效状态转换。虽然在抑制TOR激酶的细胞中观察到光合功能受损,但相同条件下会导致线粒体基础呼吸速率提高两倍,并伴随ATP产量增加。有趣的是,在抑制TOR的细胞中,这种上调的线粒体功能是由碎片化的线粒体通过上调COXIIb以及下调Hxk1和AOX1蛋白水平介导的。我们提出,TOR激酶可能作为一种传感器,在正常[具体细胞类型]细胞中对叶绿体与线粒体功能进行反向调节。

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