Differences of sexual development (DSDs) are among the most common congenital abnormalities and have long-term physical and psychological effects, but their etiology is poorly understood. In addition to a lack of knowledge of the genetic bases for most cases of DSDs, we also have a fundamental lack of understanding of the cellular interactions that promote fetal gonad formation and adult gonad homeostasis. Recent evidence from our lab and others indicates that several diverse cell types are essential for gonad differentiation and function. We are focusing on the vasculature (blood vessels) and myeloid immune cell lineage, both of which have a wide repertoire of cellular functions in development, but whose role in gonad biology is not fully appreciated.
Our lab’s goal is to elucidate the genetic and molecular mechanisms that drive the transformation of the undifferentiated gonad primordium into a sexually dimorphic and structurally specialized organ. Using the mouse as a model system, we are striving to understand the diverse cell-cell communication that occurs during gonad differentiation and homeostasis. When these signaling networks are disrupted, birth defects such as DSDs arise, as well as adult infertility. Detailed knowledge of these cellular behaviors and signaling networks will be instrumental in understanding normal human fetal development, and without such knowledge the future characterization of DSDs and infertility will likely remain a daunting endeavor. The lab’s research interests are in three main areas: fetal gonad morphogenesis, adult testis spermatogonial differentiation, and vasculature and stem cell niches.