Abstract

BackgroundSerum albumin is a key component in mammalian sperm capacitation, a functional maturation process by which sperm become competent to fertilize oocytes. Capacitation is accompanied by several cellular and molecular changes including an increased tyrosine phosphorylation of sperm proteins and a development of hyperactivated sperm motility. Both of these processes require extracellular calcium, but how calcium enters sperm during capacitation is not well understood.MethodsBSA-induced changes in intracellular calcium concentration were studied using Fluo-4 and Fura-2 calcium imaging with wild-type and Catsper1 knockout mouse sperm.ResultsWe found that the fast phase of the BSA-induced rises in intracellular calcium concentration was absent in the Catsper1 knockout sperm and could be restored by an EGFP-CATSPER1 fusion protein. The calcium concentration increases were independent of G-proteins and phospholipase C but could be partially inhibited when intracellular pH was clamped. The changes started in the principal piece and propagated toward the sperm head.ConclusionWe conclude that the initial phase of the increases in intracellular calcium concentration induced by BSA requires the CATSPER channel, but not the voltage-gated calcium channel. Our findings identify the molecular conduit responsible for the calcium entry required for the sperm motility changes that occur during capacitation.

Highlights

  • Serum albumin is a key component in mammalian sperm capacitation, a functional maturation process by which sperm become competent to fertilize oocytes

  • CATSPER channels are required for the bovine serum albumin (BSA)-induced [Ca2+]i rise in mouse sperm When applied to non-capacitated sperm lightly immobilized onto coverslips, BSA elevated [Ca2+]i in the sperm head (Figure 1A) at concentrations as low as 0.1 mg/ml (Figure 1B)

  • The major finding of our study is that CATSPER channels are required for the BSA induced [Ca2+]i increases in mouse sperm

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Summary

Introduction

Serum albumin is a key component in mammalian sperm capacitation, a functional maturation process by which sperm become competent to fertilize oocytes. Capacitation is accompanied by several cellular and molecular changes including an increased tyrosine phosphorylation of sperm proteins and a development of hyperactivated sperm motility. Both of these processes require extracellular calcium, but how calcium enters sperm during capacitation is not well understood. Sperm become capacitated in vivo, by interacting with environmental stimuli in the female reproductive tract before encountering eggs. This process can be mimicked in vitro by incubating sperm in defined capacitation media. Capacitation leads to several cellular and behavioral changes, including an increase in tyrosine phosphorylation of sperm proteins, rises in intracellular pH (pHi) and Ca2+ concentration ([Ca2+]i), membrane hyperpolarization, and hyperactivated motility [4,5,6]

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