Deciphering Conserved Genetic Pathways for Ovulation in Drosophila
Lylah Deady1, Elizabeth Knapp1, Wei Li1, Jianjun Sun*1,2
1. Department of Physiology & Neurobiology, University of Connecticut, Storrs, Connecticut 06269 USA
2. Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut 06269 USA
In the past several years, we investigated the cellular and molecular mechanisms of ovulation in Drosophila, which is proved to be highly conserved as in mammals. Drosophila oocytes are surrounded by a layer of follicle cells. During ovulation, posterior follicle cells are first degraded. The oocyte is then squeezed into the oviduct (called follicle rupture), while the rest of the follicle cells remain in the ovary to form a corpus luteum. The degradation of posterior follicle cells depends on matrix metalloproteinase 2 (Mmp2), which is specifically expressed in posterior follicle cells of all stage-14 egg chambers and whose activity is induced by octopamine (OA) signaling, equivalent to norepinephrine signaling in mammals. Parallel to progesterone in mammalian ovulation, we also showed that ecdysteroid signaling is activated in stage-14 follicle cells and essential for Drosophila ovulation. These studies led us to develop a novel ex vivo follicle rupture assay, with which we can perform RNAi-based genetic screens and identify novel follicular factors for Drosophila ovulation. I will present two novel factors (a zinc-finger transcription factor Hindsight and a NADPH oxidase), which are essential for Drosophila ovulation and likely conserved in mammalian ovulation. We are in the process of establishing a complex signaling network in follicle cells that mediate Drosophila ovulation. Ultimately, we would like to investigate the role of these novel factors in mammalian and human ovulation, which will provide a fundamental understanding of ovulation process and provide new strategies to develop novel contraceptive medicine or treat human infertile conditions.
Acknowledgements: Supported by: NIH, Gate’s foundation, and UConn to JS.
Key Words: Ovulation, steroid signaling, adrenergic signaling, transcription factor, NADPH oxidase, Drosophila
Lylah Deady1, Elizabeth Knapp1, Wei Li1, Jianjun Sun*1,2
1. Department of Physiology & Neurobiology, University of Connecticut, Storrs, Connecticut 06269 USA
2. Institute for Systems Genomics, University of Connecticut, Storrs, Connecticut 06269 USA
In the past several years, we investigated the cellular and molecular mechanisms of ovulation in Drosophila, which is proved to be highly conserved as in mammals. Drosophila oocytes are surrounded by a layer of follicle cells. During ovulation, posterior follicle cells are first degraded. The oocyte is then squeezed into the oviduct (called follicle rupture), while the rest of the follicle cells remain in the ovary to form a corpus luteum. The degradation of posterior follicle cells depends on matrix metalloproteinase 2 (Mmp2), which is specifically expressed in posterior follicle cells of all stage-14 egg chambers and whose activity is induced by octopamine (OA) signaling, equivalent to norepinephrine signaling in mammals. Parallel to progesterone in mammalian ovulation, we also showed that ecdysteroid signaling is activated in stage-14 follicle cells and essential for Drosophila ovulation. These studies led us to develop a novel ex vivo follicle rupture assay, with which we can perform RNAi-based genetic screens and identify novel follicular factors for Drosophila ovulation. I will present two novel factors (a zinc-finger transcription factor Hindsight and a NADPH oxidase), which are essential for Drosophila ovulation and likely conserved in mammalian ovulation. We are in the process of establishing a complex signaling network in follicle cells that mediate Drosophila ovulation. Ultimately, we would like to investigate the role of these novel factors in mammalian and human ovulation, which will provide a fundamental understanding of ovulation process and provide new strategies to develop novel contraceptive medicine or treat human infertile conditions.
Acknowledgements: Supported by: NIH, Gate’s foundation, and UConn to JS.
Key Words: Ovulation, steroid signaling, adrenergic signaling, transcription factor, NADPH oxidase, Drosophila