Sperm surface components involved in the control of the acrosome reaction.
Several lines of evidence suggest that decapacitation of sperm occurs normally in the male reproductive tract, and as a result the acrosome is stabilized and the acrosome reaction is controlled. Since the defining experiments in 1951, where decapacitation was reversed in the female reproductive tract by capacitation, investigations have pursued the molecular events of this process. This review attempts to examine critically the older literature and compare that perspective with the current theories. The theories for decapacitation of sperm include the possible role of a peptide decapacitation factor, a glycoprotein-mediated steroid transfer to the sperm, masking of a galactosyl transferase by some macromolecule-containing carbohydrate, preclusion of calcium influx by a binding protein, and sperm interaction with the acrosome stabilizing factor. Although these theories are diverse, there are some unifying aspects. However, there remain some major unanswered questions. For example, although we point to some circumstantial evidence that infers a single decapacitation factor, this needs to be further substantiated. It is concluded that with the purification of a macromolecule involved in capacitation, specific proposals on the mechanism of capacitation, and new tools to evaluate the capacitation process, it is likely that another decade will not pass without emergence of a unifying molecular theory of sperm capacitation.
D000177:Acrosome / Q000502:physiology*; D000818:Animals; D002417:Cattle; D002462:Cell Membrane / Q000502:physiology; D004285:Dogs; D008297:Male; D051379:Mice; D011817:Rabbits; D013075:Sperm Capacitation; D013094:Spermatozoa / Q000502:physiology*