Genomic regions responsible for manganese superoxide dismutase regulation in Drosophila melanogaster.
Genomic regions responsible for manganese superoxide dismutase regulation in Drosophila melanogaster.
复制标题
果蝇中负责锰超氧化物歧化酶调节的基因组区域。
DOI：
10.1046/j.1474-9728.2003.00056.x
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发表时间：
2003
期刊：
影响因子：
7.8
通讯作者：
Duttaroy,Atanu
中科院分区：
文献类型：
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作者：
Paul,Anirban;Duttaroy,Atanu
锰超氧化物歧化酶 (MnSOD) 的转录对于线粒体超氧自由基的解毒至关重要，已被证明在体外受到许多因素和条件的调节，包括氧化应激、细胞因子、脂多糖、细胞质 myc (c-myc)、p53 和肿瘤坏死因子。在这里，我们描述了果蝇的基因组区域，在整个生物体水平上对 MnSOD 基因的转录具有调节作用。为了了解 MnSOD 表达的整合调控，我们筛选了 D 的染色体。 黑腹细胞以找出改变 MnSOD 表达的缺陷。通过评估覆盖果蝇基因组约 81% 的 149 个缺失中 MnSOD 的相对信息丰度来筛选 MnSOD 抑制剂。染色体缺陷Df(2R)017显着上调MnSODmRNA 1.7倍。其他四个基因组区间 Df(1)ct-J4、Df(2L)BSC4、Df(3L)66C-G28 和 Df(3R)Scr 的缺陷会下调 MnSOD 表达。 MnSOD 表达的变化与缺失基因型的百草枯敏感性呈正相关。因此，果蝇基因组中存在至少一种候选增强子和四种候选抑制子来调节MnSOD基因的体内转录活性。
The transcription of manganese superoxide dismutase (MnSOD), expression of which is essential for detoxification of superoxide radicals from mitochondria, has been shown to be regulatedin vitroby many factors and conditions including oxidative stress, cytokines, lipopolysaccharide, cytoplasmic myc (c‐myc),p53and tumour necrosis factors. Here we describe genomic regions inDrosophila melanogasterwith regulatory effects on transcription of theMnSODgene at an organism‐wide level. To understand the integrated regulation ofMnSODexpression we screened chromosomes ofD. melanogasterto locate deficiencies that altered the expression ofMnSOD. Suppressors ofMnSODwere screened by assessing the relative message abundance ofMnSODin 149 deletions covering approximately 81% of theDrosophilagenome. The chromosomal deficiencyDf(2R)017significantly up‐regulatedMnSODmRNA by 1.7‐fold. Deficiency in four other genomic intervals,Df(1)ct‐J4,Df(2L)BSC4,Df(3L)66C‐G28andDf(3R)Scr, down‐regulatedMnSODexpression. Changes inMnSODexpression were positively associated with paraquat sensitivity of the deletion genotypes. Thus, at least one candidate enhancer and four candidate suppressors exist in theDrosophilagenome to regulate the transcriptional activity of theMnSODgenein vivo.