After sperm have completed their development within the testis they are released from the supporting Sertoli cells and are transported to the epididymis. This process of release from the Sertoli cell is known as spermiation and while it is well described morphologically, the molecular events controlling spermiation are unknown. Spermiation is a key factor in determining sperm counts and when spermiation failure occurs, sperm are not released from the Sertoli cell but are instead retained and phagocytosed.
We have found that spermiation failure occurs when hormone-based contraceptives are given to male rodents, monkeys and humans. Contraceptives that target spermiation would likely be rapid acting and effective and therefore elucidating the molecular pathways that control spermiation are of considerable clinical significance. This research is also relevant to developing treatments for conditions of male infertility, such as some forms of non-obstructive azoospermia.
Our group uses vivo rodent models in which spermiation is suppressed to discover which genes, proteins and molecular pathways are changed during spermiation failure. We use genome microarrays and proteomic approaches (Western blotting, DIGE and Mass Spectrometry) to discover changes in genes and proteins and investigate the localisation of spermiation-associated proteins using immunocytochemistry. We also use seminiferous tubule cultures to manipulate sperm release in vitro.