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題名 Long-lived Indy induces reduced mitochondrial reactive oxygen species production and oxidative damage
作者 Neretti, Nicola;Wang, Pei-Yu;Brodsky, Alexander S.;Nyguyen, Hieu H.;White, Kevin P.;Rogina, Blanka;Helfand, Stephen L.
王培育
Wang, Pei-Yu
貢獻者 神科所
關鍵詞 electron transport chain; mitochondria; oxidative phosphorylation; Drosophila; aging
日期 2009-02
上傳時間 21-Nov-2018 16:23:04 (UTC+8)
摘要 Decreased Indy activity extends lifespan in D. melanogaster without significant reduction in fecundity, metabolic rate, or locomotion. To understand the underlying mechanisms leading to lifespan extension in this mutant strain, we compared the genome-wide gene expression changes in the head and thorax of adult Indy mutant with control flies over the course of their lifespan. A signature enrichment analysis of metabolic and signaling pathways revealed that expression levels of genes in the oxidative phosphorylation pathway are significantly lower in Indy starting at day 20. We confirmed experimentally that complexes I and III of the electron transport chain have lower enzyme activity in Indy long-lived flies by Day 20 and predicted that reactive oxygen species (ROS) production in mitochondria could be reduced. Consistently, we found that both ROS production and protein damage are reduced in Indy with respect to control. However, we did not detect significant differences in total ATP, a phenotype that could be explained by our finding of a higher mitochondrial density in Indy mutants. Thus, one potential mechanism by which Indy mutants extend life span could be through an alteration in mitochondrial physiology leading to an increased efficiency in the ATP/ROS ratio.
關聯 Proceedings of the National Academy of Sciences of the United States of America, Vol.106, No.7, pp.2277-2282
PMID: 19164521
資料類型 article
DOI https://doi.org/10.1073/pnas.0812484106
dc.contributor 神科所
dc.creator (作者) Neretti, Nicola;Wang, Pei-Yu;Brodsky, Alexander S.;Nyguyen, Hieu H.;White, Kevin P.;Rogina, Blanka;Helfand, Stephen L.
dc.creator (作者) 王培育
dc.creator (作者) Wang, Pei-Yu
dc.date (日期) 2009-02
dc.date.accessioned 21-Nov-2018 16:23:04 (UTC+8)-
dc.date.available 21-Nov-2018 16:23:04 (UTC+8)-
dc.date.issued (上傳時間) 21-Nov-2018 16:23:04 (UTC+8)-
dc.identifier.uri (URI) http://nccur.lib.nccu.edu.tw/handle/140.119/120972-
dc.description.abstract (摘要) Decreased Indy activity extends lifespan in D. melanogaster without significant reduction in fecundity, metabolic rate, or locomotion. To understand the underlying mechanisms leading to lifespan extension in this mutant strain, we compared the genome-wide gene expression changes in the head and thorax of adult Indy mutant with control flies over the course of their lifespan. A signature enrichment analysis of metabolic and signaling pathways revealed that expression levels of genes in the oxidative phosphorylation pathway are significantly lower in Indy starting at day 20. We confirmed experimentally that complexes I and III of the electron transport chain have lower enzyme activity in Indy long-lived flies by Day 20 and predicted that reactive oxygen species (ROS) production in mitochondria could be reduced. Consistently, we found that both ROS production and protein damage are reduced in Indy with respect to control. However, we did not detect significant differences in total ATP, a phenotype that could be explained by our finding of a higher mitochondrial density in Indy mutants. Thus, one potential mechanism by which Indy mutants extend life span could be through an alteration in mitochondrial physiology leading to an increased efficiency in the ATP/ROS ratio.en_US
dc.format.extent 837146 bytes-
dc.format.mimetype application/pdf-
dc.relation (關聯) Proceedings of the National Academy of Sciences of the United States of America, Vol.106, No.7, pp.2277-2282
dc.relation (關聯) PMID: 19164521
dc.subject (關鍵詞) electron transport chain; mitochondria; oxidative phosphorylation; Drosophila; agingen_US
dc.title (題名) Long-lived Indy induces reduced mitochondrial reactive oxygen species production and oxidative damageen_US
dc.type (資料類型) article
dc.identifier.doi (DOI) 10.1073/pnas.0812484106
dc.doi.uri (DOI) https://doi.org/10.1073/pnas.0812484106