Calmodulin antagonists inhibit sea urchin sperm hyperpolarization necessary for directed movement toward the egg.

Speract, a decapeptide from Strongylocentrotus purpuratus sea urchin eggs, transiently stimulates a membrane guanylyl cyclase and activates a K(+)-selective channel that hyperpolarizes the sperm. Membrane potential recordings with fluorescent dyes in sperm flagellar vesicles were used to determine if calmodulin participates in the signal transduction induced by speract. The vesicle hyperpolarization induced by speract was inhibited by the calmodulin antagonists: trifluoperazine, mastoparan; N-(6-Aminohexyl)-5-chloro-1-naphthalenesulfonamide, (W-7); and N-(6-Aminohexyl)-1-naphthalenesulfonamide, (W-5). Since that inhibition occurred at concentrations at which calmodulin action is inhibited by these compounds, the overall findings suggested that calmodulin could be involved in the speract response. The speract response was Ca(2+)-independent however. Ten millimolar EGTA does not inhibit the hyperpolarization and 2 mM BAPTA only partially inhibited the response. High concentrations of calmodulin-dependent kinase II and phosphatase inhibitors did not alter the response of the flagella vesicles to speract. Taken as a whole, these results indicate that the speract-induced hyperpolarization involves the participation of calmodulin in a Ca2+ independent manner.