Cell-autonomous roles of theecdysonelessgene inDrosophiladevelopment and oogenesis

Abstract

Steroid signaling underlies developmental processes in animals. Mutations that impair steroidogenesis in the fruit fly Drosophila melanogasterprovide 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 ecdgene. 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.

Functional and bioinformatics analyses reveal conservation of cis‐regulatory elements between sciaridae and drosophilidae

“…This may be a consequence of the lack of data from genome-wide analyses for the ring gland, coupled to the fact that the characterization of differential patterns of gene expression in the ring gland has been impaired by the small size of this organ (Niwa et al, 2004). Most of the genes that were shown to be expressed in the ring gland are related to the ecdysone biosynthetic pathway (Freeman et al, 1999;Gaziova et al, 2004;Gilbert, 2004;Neubueser et al, 2005;Warren et al, 2001;Yoshiyama et al, 2006), and were not identified in our analysis. Because in transgenesis the pattern of BhC4-1-lacZ expression driven by the 67 bp (2253/2187) fragment is distinct from the expression pattern of the genes that participate in ecdysone biosynthesis, it is possible that our study has revealed a hitherto uncharacterized set of genes which are coexpressed in the ring gland of late embryos.…”

“…The molting defective (mld) (Neubueser et al, 2005) and without children (woc) (Warren et al, 2001) genes encode putative transcription factors that are expressed in the ring gland and several other tissues throughout development, for which the target genes have not been identified. The Drosophila genes, such as dare (Freeman et al, 1999), disembodied (dib), shadow (sad) (Gilbert, 2004), ecdysoneless (ecd1) (Gaziova et al, 2004), and neverland (nvd) (Yoshiyama et al, 2006), are all involved in ecdysteroids biosynthesis and are expressed both in the larval ring gland and in adult ovaries, which is the adult source of ecdysteroids. To our knowledge, the BhC4-1 67 bp ring gland enhancer is the only enhancer so far identified, which is able to drive developmentally regulated gene expression solely in the ring gland.…”

Ras signaling modulates activity of the ecdysone receptor EcR during cell migration in the drosophila ovary

“…2G). ecdysoneless (ecd 1 , Gaziova et al, 2004) females showed a similar eggshell phenotype when shifted to the restrictive temperature for 24 hr (Fig. 2H), indicating this phenotype is associated with reduced ecdysone signaling in the egg chamber.…”

“…At stage 8, ecdysone controls a check-point regulating egg chamber maturation. Complex interactions among genes required for ecdysteroid biosynthesis and isoforms of Br-C, Eip75B, and EcR mediate a physiological feedback to a direct a choice to develop or degenerate by apoptosis (Buszczak et al, 1999;Gaziova et al, 2004;Bownes, 2005, 2006;.…”

Sex Steroids in Insects and the Role of the Endosymbiont Wolbachia:A New Perspective

“…In other insects, the sex-specific killing action by Wolbachia occurs during embryogenesis (Dyer& Jaenike, 2004;Fialho & Stevens, 2000;Jiggins et al, 2001;Zeh et al, 2005). Embryogenesis takes place in a steroid hormone-enriched environment where steroid hormones act for the coordination of morphogenetic movements (De Loof, 2006;Kozlova & Thummel, 2003;Gaziova et al, 2004). Thus, if male-killing Wolbachia interacts with the host hormonal pathway involving ecdysteroids, this could interfere with the processes required for a normal development of males.…”