Abstract: Mechanisms of prostate development are of considerable interest to prostate biologists because signals that direct prostate morphogenesis are thought to be reactivated during prostate disease. Prostate development begins before birth when circulating androgens in the male fetus stimulate outgrowth of prostate ductal progenitors, or buds, from the urogenital sinus. Prostatic buds elongate prenatally and after birth undergo branching morphogenesis, canalization, and differentiation to create the prostate ductal network.
The aryl hydrocarbon receptor (AHR) is an orphan receptor that interfaces with multiple signaling pathways to regulate transcription. Activation of AHR signaling with the potent ligand 2,3,7,8 tetrachlordibenzo-p-dioxin (TCDD), during fetal prostate development, impairs prostatic bud formation and has an imprinting effect on the developing prostate that predisposes to prostate disease in adulthood. This research seminar will introduce the aberrant phenotype elicited by TCDD in the developing prostate and will highlight the cooperative framework of developmental signaling pathways upon which the AHR acts to regulate timing and patterning of prostatic bud formation in mice. Interactions between AHR, retinoic acid, WNT5A, and fibroblast growth factor 10 signaling pathways will be discussed.

Reception follows.