Originally published as Genetics Published Articles Ahead of Print on November 17, 2008.

Genetics, Vol. 181, 165-175, January 2009, Copyright © 2009
doi:10.1534/genetics.108.096008

Cell Survival and Polarity of Drosophila Follicle Cells Require the Activity of Ecdysone Receptor B1 Isoform

Patrizia Romani*, Fabio Bernardi*, Jennifer Hackney{dagger}, Leonard Dobens{dagger}, Giuseppe Gargiulo* and Valeria Cavaliere*,1

* Dipartimento di Biologia Evoluzionistica Sperimentale, Università di Bologna, Bologna, Italy, 40126 and {dagger} Division of Molecular Biology and Biochemistry, School of Biological Sciences, University of Missouri, Kansas City, Missouri 64110

1 Corresponding author: Dipartimento di Biologia Evoluzionistica Sperimentale, Via Selmi 3, 40126, Bologna, Italy.
E-mail: valeria.cavaliere{at}unibo.it

Proper assembly and maintenance of epithelia are critical for normal development and homeostasis. Here, using the Drosophila ovary as a model, we identify a role for the B1 isoform of the ecdysone receptor (EcR-B1) in this process. We performed a reverse genetic analysis of EcR-B1 function during oogenesis and demonstrate that silencing of this receptor isoform causes loss of integrity and multilayering of the follicular epithelium. We show that multilayered follicle cells lack proper cell polarity with altered distribution of apical and basolateral cell polarity markers including atypical-protein kinase C (aPKC), Discs-large (Dlg), and Scribble (Scrib) and aberrant accumulation of adherens junctions and F-actin cytoskeleton. We find that the EcR-B1 isoform is required for proper follicle cell polarity both during early stages of oogenesis, when follicle cells undergo the mitotic cell cycle, and at midoogenesis when these cells stop dividing and undergo several endocycles. In addition, we show that the EcR-B1 isoform is required during early oogenesis for follicle cell survival and that disruption of its function causes apoptotic cell death induced by caspase.