金属对莱茵衣藻自噬的激活作用。

Eukaryotic Cell Pub Date : 2015-09-01 Epub Date: 2015-07-10 DOI:10.1128/EC.00081-15
Marta Pérez-Martín, Crysten E Blaby-Haas, María Esther Pérez-Pérez, Ascensión Andrés-Garrido, Ian K Blaby, Sabeeha S Merchant, José L Crespo
{"title":"金属对莱茵衣藻自噬的激活作用。","authors":"Marta Pérez-Martín,&nbsp;Crysten E Blaby-Haas,&nbsp;María Esther Pérez-Pérez,&nbsp;Ascensión Andrés-Garrido,&nbsp;Ian K Blaby,&nbsp;Sabeeha S Merchant,&nbsp;José L Crespo","doi":"10.1128/EC.00081-15","DOIUrl":null,"url":null,"abstract":"<p><p>Autophagy is an intracellular self-degradation pathway by which eukaryotic cells recycle their own material in response to specific stress conditions. Exposure to high concentrations of metals causes cell damage, although the effect of metal stress on autophagy has not been explored in photosynthetic organisms. In this study, we investigated the effect of metal excess on autophagy in the model unicellular green alga Chlamydomonas reinhardtii. We show in cells treated with nickel an upregulation of ATG8 that is independent of CRR1, a global regulator of copper signaling in Chlamydomonas. A similar effect on ATG8 was observed with copper and cobalt but not with cadmium or mercury ions. Transcriptome sequencing data revealed an increase in the abundance of the protein degradation machinery, including that responsible for autophagy, and a substantial overlap of that increased abundance with the hydrogen peroxide response in cells treated with nickel ions. Thus, our results indicate that metal stress triggers autophagy in Chlamydomonas and suggest that excess nickel may cause oxidative damage, which in turn activates degradative pathways, including autophagy, to clear impaired components and recover cellular homeostasis. </p>","PeriodicalId":11891,"journal":{"name":"Eukaryotic Cell","volume":"14 9","pages":"964-73"},"PeriodicalIF":0.0000,"publicationDate":"2015-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1128/EC.00081-15","citationCount":"29","resultStr":"{\"title\":\"Activation of Autophagy by Metals in Chlamydomonas reinhardtii.\",\"authors\":\"Marta Pérez-Martín,&nbsp;Crysten E Blaby-Haas,&nbsp;María Esther Pérez-Pérez,&nbsp;Ascensión Andrés-Garrido,&nbsp;Ian K Blaby,&nbsp;Sabeeha S Merchant,&nbsp;José L Crespo\",\"doi\":\"10.1128/EC.00081-15\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Autophagy is an intracellular self-degradation pathway by which eukaryotic cells recycle their own material in response to specific stress conditions. Exposure to high concentrations of metals causes cell damage, although the effect of metal stress on autophagy has not been explored in photosynthetic organisms. In this study, we investigated the effect of metal excess on autophagy in the model unicellular green alga Chlamydomonas reinhardtii. We show in cells treated with nickel an upregulation of ATG8 that is independent of CRR1, a global regulator of copper signaling in Chlamydomonas. A similar effect on ATG8 was observed with copper and cobalt but not with cadmium or mercury ions. Transcriptome sequencing data revealed an increase in the abundance of the protein degradation machinery, including that responsible for autophagy, and a substantial overlap of that increased abundance with the hydrogen peroxide response in cells treated with nickel ions. Thus, our results indicate that metal stress triggers autophagy in Chlamydomonas and suggest that excess nickel may cause oxidative damage, which in turn activates degradative pathways, including autophagy, to clear impaired components and recover cellular homeostasis. </p>\",\"PeriodicalId\":11891,\"journal\":{\"name\":\"Eukaryotic Cell\",\"volume\":\"14 9\",\"pages\":\"964-73\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1128/EC.00081-15\",\"citationCount\":\"29\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Eukaryotic Cell\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1128/EC.00081-15\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2015/7/10 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Eukaryotic Cell","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1128/EC.00081-15","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2015/7/10 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 29

摘要

自噬是一种细胞内的自我降解途径,真核细胞通过这种途径来回收自身的物质,以应对特定的应激条件。暴露于高浓度的金属会导致细胞损伤,尽管金属胁迫对光合生物自噬的影响尚未被探索。在这项研究中,我们研究了金属过量对模型单细胞绿藻莱茵衣藻自噬的影响。我们发现,在镍处理的细胞中,ATG8的上调独立于CRR1, CRR1是衣藻中铜信号的全球调节因子。铜和钴离子对ATG8也有类似的影响,但镉或汞离子则没有。转录组测序数据显示,蛋白质降解机制的丰度增加,包括负责自噬的蛋白质,并且在镍离子处理的细胞中,这种增加的丰度与过氧化氢反应有很大的重叠。因此,我们的研究结果表明,金属应激触发了衣藻的自噬,并表明过量的镍可能导致氧化损伤,从而激活包括自噬在内的降解途径,以清除受损成分并恢复细胞稳态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

摘要图片

摘要图片

摘要图片

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
Activation of Autophagy by Metals in Chlamydomonas reinhardtii.

Autophagy is an intracellular self-degradation pathway by which eukaryotic cells recycle their own material in response to specific stress conditions. Exposure to high concentrations of metals causes cell damage, although the effect of metal stress on autophagy has not been explored in photosynthetic organisms. In this study, we investigated the effect of metal excess on autophagy in the model unicellular green alga Chlamydomonas reinhardtii. We show in cells treated with nickel an upregulation of ATG8 that is independent of CRR1, a global regulator of copper signaling in Chlamydomonas. A similar effect on ATG8 was observed with copper and cobalt but not with cadmium or mercury ions. Transcriptome sequencing data revealed an increase in the abundance of the protein degradation machinery, including that responsible for autophagy, and a substantial overlap of that increased abundance with the hydrogen peroxide response in cells treated with nickel ions. Thus, our results indicate that metal stress triggers autophagy in Chlamydomonas and suggest that excess nickel may cause oxidative damage, which in turn activates degradative pathways, including autophagy, to clear impaired components and recover cellular homeostasis.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Eukaryotic Cell
Eukaryotic Cell 生物-微生物学
自引率
0.00%
发文量
0
审稿时长
1 months
期刊介绍: Eukaryotic Cell (EC) focuses on eukaryotic microbiology and presents reports of basic research on simple eukaryotic microorganisms, such as yeasts, fungi, algae, protozoa, and social amoebae. The journal also covers viruses of these organisms and their organelles and their interactions with other living systems, where the focus is on the eukaryotic cell. Topics include: - Basic biology - Molecular and cellular biology - Mechanisms, and control, of developmental pathways - Structure and form inherent in basic biological processes - Cellular architecture - Metabolic physiology - Comparative genomics, biochemistry, and evolution - Population dynamics - Ecology
期刊最新文献
Comparison of Switching and Biofilm Formation between MTL-Homozygous Strains of Candida albicans and Candida dubliniensis. Saccharomyces cerevisiae Is Dependent on Vesicular Traffic between the Golgi Apparatus and the Vacuole When Inositolphosphorylceramide Synthase Aur1 Is Inactivated. Yeast Integral Membrane Proteins Apq12, Brl1, and Brr6 Form a Complex Important for Regulation of Membrane Homeostasis and Nuclear Pore Complex Biogenesis. Adaptations of the Secretome of Candida albicans in Response to Host-Related Environmental Conditions. Virulence-Associated Enzymes of Cryptococcus neoformans.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1