Sperm undergo capacitation while traveling through the female reproductive tract, a process including several biochemical and physiological events before fertilization. Also prior to fertilization, sperm bind to the epithelial cells of the oviduct isthmus to form a sperm reservoir. This sperm reservoir regulates sperm capacitation, reduces polyspermy and prolongs fertile lifespan. It has been proposed that oviduct glycans interact with sperm, which leads to the formation of sperm reservoir. Our lab also has previously demonstrated that porcine sperm bind to the oviductal glycans biantennary 6-sialylated Nacetyllactosamine (bi-SiaLN) oligosaccharide and a Lewis X trisaccharide (LeX) to form the sperm reservoir. These glycans are also implicated in the regulation of sperm capacitation by regulating calcium influx and extending sperm life span. My objective was to identify how sperm bound to oviduct glycans are released from the reservoir to fertilize the oocyte. The results of this study indicate that soluble oviduct glycans do not alter sperm capacitation. Progesterone and the related steroid pregnenolone release 40-60% of sperm from oviduct cells and immobilized glycans. Progesterone release requires the ion channel CatSper and protein degradation by proteasomes. Finally, the development of sperm hyperactivation was sufficient to induce sperm release, but complete release also required the function of CatSper and proteasomes. My results are the first to show that hyperactivated motility is sufficient to induce sperm release from the oviduct reservoir and implicate progesterone as an important signal to sperm promoting their release and movement towards the egg.
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