In Drosophila, ecdysone signaling is mediated by a heteromeric receptor composed of the Ecdysone Receptor protein (EcR) and the RXR homolog transcription factor Ultraspiracle (USP). There are three different EcR isoforms: EcR-A, EcR-B1 and EcR-B2 that differ in their N termini and have different spatial–temporal functions. Here we analized the effects of EcR-B1 or USP loss of function in the follicular epithelium during oogenesis. We find that targeting RNAi of EcR-B1 by using the ubiquitous Tubulin-Gal4 driver causes severe alteration in egg chamber development. Silencing of EcR-B1 isoform in flp-out clones causes apoptotic follicle cell death and affects follicular epithelium monolayer structure. Multilayered follicle cells are also detected knocking down EcR-B1 isoform by using enhancer trap lines that drive Gal4 expression at mid-oogenesis. We show that multilayered follicle cells lack proper cell polarity with altered distribution of apical and baso-lateral cell polarity markers (atypical-PKC, Armadillo, Discs-large and Scribble). Furthermore, these delaminating follicle cells show accumulation of adherens junctions (DE-Cadherin) and their F-actin cytoskeleton is strongly affected. Interestingly, we found that mosaic follicle cells homozigous for the usp3 mutation that interferes with USP repressor activity die by apoptosis at early stages of oogenesis and show only slightly increased Discs-large expression levels but not alteration in DE-cadherin expression levels. These data indicate that follicular epithelium morphogenesis and follicle cell survival require EcR-B1 and USP activities.

Novel functions of Ecdysone receptor B1 isoform during Drosophila oogenesis

ROMANI, PATRIZIA;BERNARDI, FABIO;DUCHI, SERENA;GARGIULO, GIUSEPPE;CAVALIERE, VALERIA
2008

Abstract

In Drosophila, ecdysone signaling is mediated by a heteromeric receptor composed of the Ecdysone Receptor protein (EcR) and the RXR homolog transcription factor Ultraspiracle (USP). There are three different EcR isoforms: EcR-A, EcR-B1 and EcR-B2 that differ in their N termini and have different spatial–temporal functions. Here we analized the effects of EcR-B1 or USP loss of function in the follicular epithelium during oogenesis. We find that targeting RNAi of EcR-B1 by using the ubiquitous Tubulin-Gal4 driver causes severe alteration in egg chamber development. Silencing of EcR-B1 isoform in flp-out clones causes apoptotic follicle cell death and affects follicular epithelium monolayer structure. Multilayered follicle cells are also detected knocking down EcR-B1 isoform by using enhancer trap lines that drive Gal4 expression at mid-oogenesis. We show that multilayered follicle cells lack proper cell polarity with altered distribution of apical and baso-lateral cell polarity markers (atypical-PKC, Armadillo, Discs-large and Scribble). Furthermore, these delaminating follicle cells show accumulation of adherens junctions (DE-Cadherin) and their F-actin cytoskeleton is strongly affected. Interestingly, we found that mosaic follicle cells homozigous for the usp3 mutation that interferes with USP repressor activity die by apoptosis at early stages of oogenesis and show only slightly increased Discs-large expression levels but not alteration in DE-cadherin expression levels. These data indicate that follicular epithelium morphogenesis and follicle cell survival require EcR-B1 and USP activities.
Ecdysone Workshop 2008
97
97
Romani P.; Bernardi F.; Duchi S.; Hackney J.; Dobens L.; Gargiulo G.; Cavaliere V.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/64405
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