Abstract
A temperature-sensitive lethal mutant of Drosophila melanogaster called ecd1 becomes deficient in ecdysone, as measured by a radioimmunoassay, when there is a shift in temperature from 20° to 29° at various stages of development. Associated with the ecdysone deficiency at 29°, there are abnormalities in larval and imaginal development and the adult functions. When the shift occurs early in third-instar stage, the mutant larvae grow to full size but fail to pupariate, and instead remain living larvae for as long as 3 weeks. These larvae, which have only about 5% as much ecdysone as the wild-type at the time of pupariation, can be induced to pupariate at 29° by ecdysone in their food, indicating that the pupariation block results from an ecdysone deficiency. A shift to 29° later in the third-instar stage does not prevent pupariation of the mutant, but the imaginal discs fail to complete differentiation, although the discs can differentiate at 29° after transplantation to the normal environment of a wild-type host. A shift to 29° early in the first-instar stage blocks a subsequent rise in ecdysone titer and results in extensive developmental defects. Mutant adults become sterile at 29°, and the ecdysone titer in the females concomitantly decreases to 13% of the wild-type value. Mutant larval ovaries transplanted to wild-type female hosts continue to develop and produce competent eggs at 20°, but when the adult hosts are put at 29° the transplanted ovaries become sterile, suggesting that the ecdysone needed for female fertility is synthesized autonomously by ovarian tissue. In contrast to these effects of a shift to 29° during larval, pupal, and adult stages, there is a normal increase in ecdysone titer and normal development in mutant embryos grown at 29°. The insensitivity of the embryo to the ecd1 mutation might be due to a maternal contribution of components needed for ecdysone synthesis during the embryonic stage.
Keywords: steroid hormone, temperature-sensitive mutants
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Selected References
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