{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T10:31:48Z","timestamp":1790937108594,"version":"4.1.0"},"reference-count":80,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2007,4,13]],"date-time":"2007-04-13T00:00:00Z","timestamp":1176422400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2007,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Ecdysone Receptor (EcR) mediates effects of the hormone ecdysone during larval molts, pupal metamorphosis, and adult female oogenesis. In the ovary, egg chamber formation requires interactions between the somatic follicle cell (FC) epithelium and the germ line nurse cell\/oocyte cyst. Previous work has shown EcR is required in the germ line for egg chamber maturation, and here we examine EcR requirements in the FC at late stages of oogenesis. EcR protein is ubiquitous in the FC but its activity is restricted, visualized by activity of the \u201cligand sensor\u201d hs\u2010GAL4\u2010EcR ligand binding domain fusion and <jats:italic>EcRE\u2010lacZ<\/jats:italic> reporter gene expression. GAL4\u2010EcR is activated in the FC by an ecdysone agonist and repressed by tissue\u2010specific Ras GTPase signals. To determine the significance of restricted sites of EcR activity in the FC, we used targeted misexpression of the dominant negative EcR (EcR\u2010DN) molecules EcR<jats:sup>F645A<\/jats:sup> and EcR<jats:sup>W650A<\/jats:sup>. EcR\u2010DN expression at stage 10 reduced <jats:italic>EcRE\u2010lacZ<\/jats:italic> expression in the nurse cell FC and resulted in abnormal FC migrations, including aberrant centripetal migration and dorsal appendage tube formation, leading to the formation of cup\u2010shaped eggs with shortened, branched dorsal appendages at stage 14. Clones of FC expressing EcR\u2010DN displayed cell\u2010autonomous increases in DE\u2010cadherin expression and abnormal epithelial junction formation. EcR\u2010DN expression caused thin eggshell phenotypes that correlated with both reduced levels of chorion gene expression and reduction in chorion gene amplification. Our results indicate that tissue\u2010specific modulation of EcR activity by the Ras signaling pathway refines temporal ecdysone signals that regulate FC differentiation and cadherin\u2010mediated epithelial cell shape changes. Developmental Dynamics 236:1213\u20131226, 2007. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.21140","type":"journal-article","created":{"date-parts":[[2007,4,13]],"date-time":"2007-04-13T11:47:01Z","timestamp":1176464821000},"page":"1213-1226","source":"Crossref","is-referenced-by-count":74,"title":["Ras signaling modulates activity of the ecdysone receptor EcR during cell migration in the drosophila ovary"],"prefix":"10.1002","volume":"236","author":[{"given":"Jennifer 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