Joan Jorgensen
Job Description
Disruptions in cell-cell interactions and signaling during fetal development can result in obvious birth defects, but more subtle deficiencies are increasingly being recognized as manifesting in diseases that are not recognized until much later in life. My laboratory’s investigations into female and male gonad development are inspired by the quest to understand the fetal basis of sex-specific adult diseases in reproductive endocrinology. Our interest in female gonad development is focused on formation of the unique cellular niche, the follicle, which ensures survival and maturation of the female gamete. We discovered a cluster of homeobox transcription factors that are expressed during ovary development whose disruption results in follicle failure and oocyte death, classic components of premature ovarian failure, a devastating disease that leads to premature menopause in adult females. Our interest in male gonad development is centered on local regulation of androgen synthesis. A fundamental difference in male versus female sex differentiation in mammalian species is that only the male fetus produces hormones: androgens. Studies show that optimal development of the mammalian male reproductive tract requires exquisite timing and critical thresholds of androgen production, but little is known about how this is controlled. Indeed, defective androgen synthesis or activity during fetal development is emerging as a component of adult male infertility and decreased virility. Thus, the major goals of my research are to discover local cell-cell interactions and molecular mechanisms that are used to establish the nascent ovarian follicle niche within the developing ovary, and that control the onset and maintenance of fetal testosterone synthesis in the developing testis.
