| Literature DB >> 25057436 |
Thanh Binh Nguyen1, Hiroyuki Ida2, Mai Shimamura2, Daishi Kitazawa2, Shinichi Akao2, Hideki Yoshida3, Yoshihiro H Inoue4, Masamitsu Yamaguchi3.
Abstract
In man, COX (cytochrome c oxidase) deficiency is reported to be related to mutation of the SCO2 (synthesis of cytochrome c oxidase 2) gene, which encodes one of the copper-donor chaperones involved in the assembly of mitochondrial cytochrome c oxidase. Such COX deficiency due to the genetic condition leads to heart disease and the Leigh syndrome and is frequently fatal in childhood. Synthesis of cytochrome c oxidase X (SCOX) is a Drosophila orthologue of human SCO2. Here, we generated SCOX-knockdown flies and the full length SCOX transgenic flies to investigate the in vivo roles of SCOX. Our results demonstrated knockdown of SCOX gene in all cells and tissues to be associated with lethality at larval or pupal stages and this correlated with a decrease in ATP level. In contrast, the full length SCOX transgenic flies showed a longer lifespan than wild type flies and control flies carrying Act5C-GAL4 alone and this correlated with an increase in ATP level. Finally, when cultured on paraquat-added medium, full length SCOX transgenic flies also exhibited an elongated lifespan. Therefore, we hypothesized that SCOX plays an important role in ATP production and consumption, which helps to prevent production of mitochondrial reactive oxygen species and/or impairment of mitochondrial activity under oxidative stress.Entities:
Keywords: ATP; COX; ROS; SCO2; SCOX; lifespan
Year: 2014 PMID: 25057436 PMCID: PMC4106651
Source DB: PubMed Journal: Am J Cancer Res ISSN: 2156-6976 Impact factor: 6.166