Disorders 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 testis formation and adult testis homeostasis. Recent evidence from our lab and others indicates that several diverse cell types are essential for testis differentiation and function. We are focusing on the myeloid immune cell lineage, which has a wide repertoire of cellular functions in development, but whose role in testis 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 two main areas: fetal testis morphogenesis and adult testis spermatogonial differentiation.