Belton Amy, Paul Anirban, Duttaroy Atanu
Biology Department, Howard University, Washington DC 20059, USA.
Genome. 2006 Jul;49(7):746-51. doi: 10.1139/g06-029.
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.
我们获得了两个缺失片段，即Df(2R)Sod2 - 11和Df(2R)Sod2 - 332，它们包含果蝇中的锰超氧化物歧化酶（MnSOD）基因或一个被称为SOD2n283的无效突变体。分子分析表明，Df(2R)Sod2 - 332缺失完全覆盖了MnSOD及其相邻基因Arp53D，而Df(2R)Sod2 - 11缺失了MnSOD基因的启动子区域。由于MnSOD表达降低，这些缺失杂合子现在对氧化应激敏感。与最近在53C/D区域获得的一些缺失进行互补分析表明，该区间存在其他必需基因座，其次，Arp53D功能对于生物体的存活并非必需。这些缺失将有助于在MnSOD肽中恢复错义替代，并研究它们对氧化应激抗性的影响。
