Speract, a sea urchin egg peptide that regulates sperm motility, also stimulates sperm mitochondrial metabolism

• Speract increases NADH levels and depolarizes the sea urchin sperm mitochondrion.
• The pHi increase triggered by speract finely coordinates the changes in ΔΨ and NADH.
• The speract-induced NADH rise and the ΔΨ decrease depend mainly on CPT-I activity.

Sea urchin sperm have only one mitochondrion, that in addition to being the main source of energy, may modulate intracellular Ca2 + concentration ([Ca2 +]i) to regulate their motility and possibly the acrosome reaction. Speract is a decapeptide from the outer jelly layer of the Strongylocentrotus purpuratus egg that upon binding to its receptor in the sperm, stimulates sperm motility, respiration and ion fluxes, among other physiological events. Altering the sea urchin sperm mitochondrial function with specific inhibitors of this organelle, increases [Ca2 +]i in an external Ca2 + concentration ([Ca2 +]ext)-dependent manner (Ardón, et al., 2009. BBActa 1787: 15), suggesting that the mitochondrion is involved in sperm [Ca2 +]i homeostasis. To further understand the interrelationship between the mitochondrion and the speract responses, we measured mitochondrial membrane potential (ΔΨ) and NADH levels. We found that the stimulation of sperm with speract depolarizes the mitochondrion and increases the levels of NADH. Surprisingly, these responses are independent of external Ca2 + and are due to the increase in intracellular pH (pHi) induced by speract. Our findings indicate that speract, by regulating pHi, in addition to [Ca2 +]i, may finely modulate mitochondrial metabolism to control motility and ensure that sperm reach the egg and fertilize it.