Inagaki H, Matsushima Y, Ohshima M, Kitagawa Y
Graduate Program of Biochemical Regulation, Graduate School of Agricultural Sciences, Nagoya University, Japan.
J Interferon Cytokine Res. 1997 May;17(5):263-9. doi: 10.1089/jir.1997.17.263.
Mitochondrial gene transcription activity in organello was suppressed after culturing HeLa cells with 1000 U/ml of interferon-alpha (IFN-alpha) or IFN-gamma for 18 h. The suppression was associated with reduced levels of mitochondrial gene transcripts. Northern blot analysis of HeLa cell RNA showed marked reduction of the mRNA encoding for mitochondrial transcription factor A (mtTFA). Immunoblotting with antiserum directed against recombinant mtTFA showed a reduced level of the protein as well. Consistently, gel-retardation assay of mitochondrial extract showed reduced level of functional mtTFA, which is known to bind to both heavy and light strand promoters of bidirectionally transcribed mitochondrial DNA. We suggest that depletion of mtTFA is a pathway through which IFNs depress the mitochondrial respiration.
用1000 U/ml的α干扰素（IFN-α）或γ干扰素培养HeLa细胞18小时后，线粒体基因在细胞器中的转录活性受到抑制。这种抑制与线粒体基因转录本水平降低有关。对HeLa细胞RNA进行的Northern印迹分析显示，编码线粒体转录因子A（mtTFA）的mRNA显著减少。用针对重组mtTFA的抗血清进行免疫印迹分析也显示该蛋白水平降低。同样，线粒体提取物的凝胶阻滞分析表明，功能性mtTFA水平降低，已知mtTFA可与双向转录的线粒体DNA的重链和轻链启动子结合。我们认为，mtTFA的耗竭是干扰素抑制线粒体呼吸的一条途径。
