Cell-autonomous roles of the ecdysoneless gene in Drosophila development and oogenesis (original) (raw)
RESEARCH ARTICLE| 01 June 2004
1Department of Molecular Biology, University of South Bohemia, and Institute of Entomology ASCR, Ceske Budejovice 37005, Czech Republic
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2Department of Biology, University of North Carolina Greensboro, Greensboro, NC 27402, USA
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2Department of Biology, University of North Carolina Greensboro, Greensboro, NC 27402, USA
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1Department of Molecular Biology, University of South Bohemia, and Institute of Entomology ASCR, Ceske Budejovice 37005, Czech Republic
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Ivana Gaziova
1Department of Molecular Biology, University of South Bohemia, and Institute of Entomology ASCR, Ceske Budejovice 37005, Czech Republic
Peter C. Bonnette
2Department of Biology, University of North Carolina Greensboro, Greensboro, NC 27402, USA
Vincent C. Henrich
2Department of Biology, University of North Carolina Greensboro, Greensboro, NC 27402, USA
Marek Jindra*
1Department of Molecular Biology, University of South Bohemia, and Institute of Entomology ASCR, Ceske Budejovice 37005, Czech Republic
Online ISSN: 1477-9129
Print ISSN: 0950-1991
Development (2004) 131 (11): 2715–2725.
Steroid signaling underlies developmental processes in animals. Mutations that impair steroidogenesis in the fruit fly _Drosophila melanogaster_provide tools to dissect steroid hormone action genetically. The widely used temperature-sensitive mutation ecdysoneless1(ecd1) disrupts production of the steroid hormone ecdysone, and causes developmental and reproductive defects. These defects cannot be satisfactorily interpreted without analysis of the _ecd_gene. Here, we show that ecd encodes an as yet functionally undescribed protein that is conserved throughout eukaryotes. The ecd1 conditional allele contains an amino acid substitution, whereas three non-conditional larval lethal mutations result in truncated Ecd proteins. Consistent with its role in steroid synthesis, Ecd is expressed in the ecdysone-producing larval ring gland. However, development of _ecd_-null early larval lethal mutants cannot be advanced by Ecd expression targeted to the ring gland or by hormone feeding. Cell-autonomous ecd function, suggested by these experiments, is evidenced by the inability of ecd– clones to survive within developing imaginal discs. Ecd is also expressed in the ovary, and is required in both the follicle cells and the germline for oocyte development. These defects, induced by the loss of ecd, provide the first direct evidence for a cell-autonomous function of this evolutionarily conserved protein.
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