Roles of ecdysone in Drosophila development
- 1 November 1977
- journal article
- research article
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 74 (11), 5099-5103
- https://doi.org/10.1073/pnas.74.11.5099
Abstract
A temperature-sensitive lethal mutant of D. melanogaster called ecd1 becomes deficient in ecdysone, as measured by a radioimmunoassay, when there is a shift in temperature from 20.degree. to 29.degree. C at various stages of development. Associated with the ecdysone deficiency at 29.degree. C there are abnormalities in larval and imaginal development and the adult functions. When the shift occurs early in 3rd-instar stage, the mutant larvae grow to full size but fail to pupariate, and instead remain living larvae for as long as 3 wk. 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.degree. C by ecdysone in their food, indicating that the pupariation block results from an ecdysone deficiency. A shift to 29.degree. C later in the 3rd-instar does not prevent pupariation of the mutant, but the imaginal discs fail to complete differentiation, although the discs can differentiate at 29.degree. C after transplantation to the normal environment of a wild-type host. A shift to 29.degree. C early in the 1st-instar stage blocks a subsequent rise in ecdysone titer and results in extensive developmental defects. Mutant adults become sterile at 29.degree., 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.degree. C, but when the adult hosts are put at 29.degree. C 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.degree. C during larval, pupal and adult stages, there is a normal increase in ecdysone titer and normal development in mutant embryos grown at 29.degree. . 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
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