Title: Regulation of Protein Phosphorylation during Sperm Capacitation1
Abstract: After leaving the testis, mammalian spermatozoa from many species are morphologically differentiated but have acquired neither progressive motility nor the ability to fertilize a metaphase II-arrested egg. During epididymal transit, sperm acquire the ability to move progressively; however, they are still fertilization incompetent. Fertilization capacity is gained after residence in the female tract for a finite period of time. The physiological changes that confer on the sperm the ability to fertilize are collectively called ‘‘capacitation.’’ Capacitation was first described and defined independently by Chang [1, 2] and Austin [3, 4]. The definition of this poorly understood phenomenon has been modified and narrowed over the years. Although fertilization still represents the benchmark endpoint of a capacitated sperm, the ability of the sperm to undergo a regulated acrosome reaction (e.g., in response to the zona pellucida) can be taken as an earlier, upstream endpoint of this extratesticular maturational event. It must be stressed at this point that capacitation is also correlated with changes in sperm motility patterns, designated as sperm hyperactivation, in a number of species [5, 6]. There are examples of cases in which capacitation and hyperactivation can be dissociated experimentally [7], but one cannot yet argue that hyperactivation of motility represents an event completely independent of the capacitation process [6]. Therefore, when one attempts to understand the process of capacitation at the molecular level, it is necessary to consider events occurring both in the head (i.e., acrosome reaction) and in the tail (i.e., motility changes). The physiological site of capacitation in vivo is the oviduct or the uterus, depending on the species [5]. However, capacitation in vitro has been accomplished using cauda and/or ejaculated sperm incubated under a variety of conditions in defined media that mimic the electrolyte composition of the oviduct fluid. In most cases, these media contain energy substrates such as pyruvate, lactate, and glucose (depending on the species); a protein source that usually is serum albumin; NaHCO3; and Ca21. The action of these media components to promote capacitation at the molecular level is poorly understood and will be discussed in this review. This review is not intended to provide an ex-