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Roles of Ecdysone in Drosophila Development

Alan Garen, Lawrence Kauvar and Jean-Antoine Lepesant
Proceedings of the National Academy of Sciences of the United States of America
Vol. 74, No. 11 (Nov., 1977), pp. 5099-5103
Stable URL: http://www.jstor.org/stable/67534
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Roles of Ecdysone in Drosophila Development
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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 degrees to 29 degrees at various stages of development. Associated with the ecdysone deficiency at 29 degrees, 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 degrees by ecdysone in their food, indicating that the pupariation block results from an ecdysone deficiency. A shift to 29 degrees 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 degrees after transplantation to the normal environment of a wild-type host. A shift to 29 degrees 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 degrees, 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 degrees, but when the adult hosts are put at 29 degrees 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 degrees during larval, pupal, and adult stages, there is a normal increase in ecdysone titer and normal development in mutant embryos grown at 29 degrees. 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.

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