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Regulatory cis- and trans-elements of mitochondrial D-loop-driven reporter genes in budding tunicates

机译:线粒体D-LOP驱动的报告基因的调节顺式和反式元素在萌芽外观

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摘要

To unveil the underlying mechanism of mitochondrial gene regulation associated with ageing and budding in the tunicate Polyandrocarpa misakiensis, mitochondrial non-coding-region (NCR)-containing reporter genes were constructed. PmNCR2.3K/GFP was expressed spatiotemporally in a pattern quite similar to mitochondrial 16S rRNA. The reporter gene expression was sensitive to high dose of rifampicin similar to mitochondrial genes, suggesting that the transcription indeed occurs in mitochondria. However, the gene expression also occurred in vivo in the cell nucleus and in vitro in the nuclear extracts. Mitochondria) transcription factor A (PmTFAM) enhanced reporter gene expression, depending on the NCR length. A budding-specific polypeptide TC14-3 is an epigenetic histone methylation inducer. It heavily enhanced reporter gene expression that was interfered by histone methylation inhibitors and PmTFAM RNAi. Our results indicate for the first time that the nuclear histone methylation is involved in mitochondrial gene activity via TFAM gene regulation.
机译:为了揭示与衰老和衰老相关的线粒体基因调节的潜在机制,并在剧烈的polyborocarpa misakiensis中,构建了线粒体非编码区(NCR)的报告基因。 PMNCR2.3K / GFP以与线粒体16S rRNA非常相似的图案表达瞬发血模。报告基因表达对类似于线粒体基因的高剂量利福平表达敏感,表明转录确实发生在线粒体中。然而,基因表达也存在于细胞核中的体内和核提取物中的体外。线粒体)转录因子A(PMTFAM)增强的报告基因表达,取决于NCR长度。特异性多肽TC14-3是表观遗传组蛋白甲基化诱导剂。它严重增强了通过组蛋白甲基化抑制剂和PMTFAM RNAi干扰的报告基因表达。我们的结果表明,核组蛋白甲基化首次通过TFAM基因调控参与线粒体基因活性。

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