Mouse oocyte maturation: How similar is it to frog oocyte maturation?

Abstract

In this study, I have attempted to address the similarities/differences between amphibian and mouse oocytes by focusing on two aspects of mouse oocyte maturation. In the first project, I investigated the ability of several antagonists of serotonin receptors to initiate follicle-enclosed mouse oocytes to undergo maturation. I demonstrated that ritanserin, but not any others, was capable of inducing oocyte maturation in the intact mouse follicles. Significantly, ritanserin is also capable of inducing frog oocyte maturation, as demonstrated by others in our lab. These results therefore suggested that a similar cAMP-elevating G protein coupled receptor, the target of ritanserin, is responsible for maintaining prophase arrest in both frog and mouse oocytes. In the second project, I have investigated the ability brefeldin A (BFA), a specific inhibitor of a small G protein ARF1, to initiate mouse oocyte maturation, as it has been suggested that BFA is capable of inducing frog oocyte maturation. I demonstrated that BFA indeed was as potent as human chorionic gonadotropin (HCG) to initiate follicle-enclosed oocytes to undergo germinal vesicle breakdown. However, BFA-treated oocytes failed to complete maturation and, instead, were arrested at metaphase I with apparently normal bipolar spindles. We further demonstrated a dominant negative mutant of ARF1 (ARF1-T31N-HA) similarly arrested the maturing oocytes at metaphase I. These studies helped reinforce the idea that oocyte maturation is fundamentally the same in mammals as it is in amphibians. The experimentally observed differences may not be very significant biologically. This concept will be discussed in conjunction with recently published literature. (Abstract shortened by UMI.)