Matsubayashi H, Tobari Y N, Hori S H
Department of Biology, Faculty of Science, Tokyo Metropolitan University, Japan.
Jpn J Genet. 1991 Aug;66(4):387-97. doi: 10.1266/jjg.66.387.
The Om(2D)63 mutants were mutagenized by gamma-ray irradiation and DEB feeding. A total of nine revertants were recovered and characterized; eight revertants were homozygous-lethal expressing no appreciable abnormality in cuticular pattern and central nervous system, and all failed to complement the lethality with each other. Two of the eight expressed embryonic lethality and were associated with cytologically detectable deletions including the putative Om(2D) locus, while four were associated with rearrangements in a region distal to the insertion sites of the tom elements. No rearrangement was detected in the remaining two by Southern blot analysis. One of the nine revertants was homozygous-viable with wild-type eyes and was associated with a reciprocal translocation with the break points at 48B in 2R (Om(2D) locus) and 96A in 3R. Based on these data, it is concluded that interaction between the region comprised of a single complementation group of the recessive lethal and the inserted tom elements seems to be responsible for the Om(2D) mutant phenotype. In addition, two induced dominant enhancers specific to Om(2D)63 were identified; both mapped on chromosome 2.
通过γ射线照射和二乙基亚硝胺（DEB）喂养对Om(2D)63突变体进行诱变。共获得9个回复体并进行了表征；8个回复体为纯合致死，在表皮模式和中枢神经系统中未表现出明显异常，且彼此之间均无法互补致死性。8个回复体中有2个表现出胚胎致死性，与细胞学可检测到的缺失相关，包括假定的Om(2D)位点，而4个与tom元件插入位点远端区域的重排相关。通过Southern印迹分析，在其余2个回复体中未检测到重排。9个回复体中有1个是具有野生型眼睛的纯合可育体，与一个相互易位相关，断点分别位于2R的48B（Om(2D)位点）和3R的96A。基于这些数据，得出结论：由隐性致死的单个互补群组成的区域与插入的tom元件之间的相互作用似乎是Om(2D)突变体表型的原因。此外，还鉴定出两个特定于Om(2D)63的诱导型显性增强子；两者均定位于2号染色体上。
