Abstract

The NR5A-family nuclear receptors are highly conserved and function within the somatic follicle cells of the ovary to regulate folliculogenesis and ovulation in mammals; however, their roles in Drosophila ovaries are largely unknown. Here, we discover that Ftz-f1, one of the NR5A nuclear receptors in Drosophila, is transiently induced in follicle cells in late stages of oogenesis via ecdysteroid signaling. Genetic disruption of Ftz-f1 expression prevents follicle cell differentiation into the final maturation stage, which leads to anovulation. In addition, we demonstrate that the bHLH/PAS transcription factor Single-minded (Sim) acts as a direct target of Ftz-f1 to promote follicle cell differentiation/maturation and that Ftz-f1's role in regulating Sim expression and follicle cell differentiation can be replaced by its mouse homolog steroidogenic factor 1 (mSF-1). Our work provides new insight into the regulation of follicle maturation in Drosophila and the conserved role of NR5A nuclear receptors in regulating folliculogenesis and ovulation.

Highlights

  • IntroductionAn essential half of the reproductive equation, requires proper follicle maturation and ovulation

  • Female fertility, an essential half of the reproductive equation, requires proper follicle maturation and ovulation

  • We demonstrate that Ftz-f1 is transiently expressed in Drosophila follicle cells at stages 10B-12 and this expression is induced by ecdysteroid signaling in stage-10B follicle cells, independent of Ttk69

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Summary

Introduction

An essential half of the reproductive equation, requires proper follicle maturation and ovulation. The majority of what is known concerning these NR5A receptors in female fertility stems from studies performed over the past two decades in rodent models. These investigations have shown that both members of this family, NR5A1 (steroidogenic factor-1 or SF-1) and NR5A2 (liver receptor homolog-1 or LRH-1), are expressed in the follicle cells that encapsulate the oocyte throughout oogenesis (Falender et al, 2003; Hinshelwood et al, 2003). Much less is known about the molecular mechanism of SF-1 in these ovarian follicle cells

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