Nishimura Kenji, Nakagawa Reiko, Hachisuga Chisato, Nakajima Munekage Yuri
Department of Bioscience, School of Science and Technology, Kwansei Gakuin University, Sanda 669-1337, Hyogo, Japan.
Laboratory for Phyloinformatics in RIKEN Center for Biosystems Dynamics Research (BDR), Kobe 650-0047, Hyogo, Japan.
Plants (Basel). 2021 Mar 10;10(3):519. doi: 10.3390/plants10030519.
Here, we explored heat dependent thylakoid FtsH protease substrates and investigated proteotoxicity induced by thermal damage and processive protease dysfunction on the thylakoid membrane. Through our thylakoid enriched proteome analysis and biochemical experiments, carbonylated stromal proteins were suggested as possible FtsH targets. Furthermore, we observed in the thylakoid fractions in the absence of FtsH stromal reactive oxygen species-detoxifying enzymes, as well as heat shock proteins and chaperones, which are known to be upregulated at the transcriptional level when this protease is absent, which is called the damaged protein response, resembling unfolded protein response in eukaryotic cells. Interestingly, the thylakoid-enriched high-density fractions included stromal translation factors and RNA-binding proteins, along with aminoacyl-tRNA synthetase, reminiscent of the formation of stress granules. Unexpectedly, extraplastid proteins such as mitochondrial chaperones, peroxidase, tricarboxylic acid cycle and respiratory chain enzymes, as well as cytosolic ribosomes, translation factors, heat shock proteins, antioxidants and metabolic enzymes, were also found deposited in the high-density fractions depending on the loss of thylakoid FtsH, with more prominent effects of thermal stress on the cytosolic proteins. This may reflect intracellular adaptation to the proteotoxic influences from the organelle.
在此,我们探索了热依赖型类囊体FtsH蛋白酶底物,并研究了热损伤和类囊体膜上持续性蛋白酶功能障碍所诱导的蛋白毒性。通过我们的类囊体富集蛋白质组分析和生化实验,羰基化的基质蛋白被认为是可能的FtsH靶点。此外,我们在缺乏FtsH的类囊体组分中观察到基质活性氧解毒酶、热休克蛋白和伴侣蛋白,已知当这种蛋白酶缺失时,这些蛋白会在转录水平上调,这被称为损伤蛋白反应,类似于真核细胞中的未折叠蛋白反应。有趣的是,类囊体富集的高密度组分中包括基质翻译因子和RNA结合蛋白,以及氨酰-tRNA合成酶,这让人联想到应激颗粒的形成。出乎意料的是,还发现线粒体伴侣蛋白、过氧化物酶、三羧酸循环和呼吸链酶等质体外蛋白,以及胞质核糖体、翻译因子、热休克蛋白、抗氧化剂和代谢酶,也会根据类囊体FtsH的缺失而沉积在高密度组分中,热应激对胞质蛋白的影响更为显著。这可能反映了细胞内对来自细胞器的蛋白毒性影响的适应性。