Deletions encompassing the manganese superoxide dismutase gene in the Drosophila melanogaster genome
Deletions encompassing the manganese superoxide dismutase gene in the Drosophila melanogaster genome
复制标题
DOI：
10.1139/g06-029
复制
发表时间：
2006-07-01
期刊：
影响因子：
3.1
通讯作者：
Duttaroy, Atanu
中科院分区：
文献类型：
--
作者：
Belton, Amy;Paul, Anirban;Duttaroy, Atanu
Df（2R）Sod2 - 11和Df（2R）Sod2 - 332两个缺失被回收，其包含果蝇中的锰超氧化物歧化酶（MnSOD）基因或称为SOD2n283的无效突变体。分子生物学分析表明，Df（2R）Sod2 - 332缺失完全暴露了MnSOD及其邻近基因Arp53D，而Df（2R）Sod2 - 11缺失了MnSOD基因的启动子区。作为MnSOD表达减少的结果，这些缺失杂合子现在对氧化应激敏感。互补分析与一些最近恢复的缺失在53 C/D区域已经建立了其他必要的基因座存在于这一区间，第二，Arp53 D功能是不是必不可少的生存的有机体。这些缺失将有助于恢复MnSOD肽中的错义取代及其对氧化应激抗性的影响。
Two deletions, Df(2R)Sod2-11 and Df(2R)Sod2-332, are recovered that encompass the manganese superoxide dismutase (MnSOD) gene or a null mutant referred to as SOD2n283 in Drosophila. Molecular analysis has revealed that the Df(2R)Sod2-332 deletion completely uncovered both MnSOD and its adjacent gene, Arp53D, whereas Df(2R)Sod2-11 was missing the promoter region of MnSOD gene. As a consequence of reduced MnSOD expression, these deletion heterozygotes are now sensitive to oxidative stress. Complementation analysis with some recently recovered deletions in the 53C/D region has established that other essential loci exist in this interval, and second, that Arp53D function is not essential for the survival of the organism. These deletions will be instrumental in the recovery of missense substitutions in the MnSOD peptide and their influence on oxidative stress resistance.