Abstract
The eggs produced by deep orange females (dor/dor) of Drosophila melanogaster have a defect that causes early death of the deep orange embryos derived from these eggs. Ovaries transplanted from deep orange females to normal female hosts continue to produce defective eggs, showing that the dor mutation directly affects an ovarian function. In heterozygous embryos (dor+/dor) derived from eggs of deep orange females, the presence of a paternal dor+ gene enables normal development to occur in about half of the embryos. Thus, the egg defect caused by the dor mutation is repairable after fertilization by the action of a dor+ gene.
The deep orange egg defect has also been repaired by injection of cytoplasm from unfertilized normal eggs into deep orange embryos at the syncitial preblastoderm stage of development. About one-third of the injected deep orange embryos were able to continue their development to an advanced stage of embryogenesis. This developmental response can serve as a bioassay for the identification of the defective component in eggs of deep orange females.
Keywords: developmental genetics, maternal effect mutations
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Selected References
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