Referenced in: none

Automatically associated channels: Slo1 , Slo3

Title: SLO3 K+ channels control calcium entry through CATSPER channels in sperm.

Authors: Julio César Chávez, Juan José Ferreira, Alice Butler, José Luis De La Vega Beltrán, Claudia L Treviño, Alberto Darszon, Lawrence Salkoff, Celia M Santi

Journal, date & volume: J. Biol. Chem., 2014 Nov 14 , 289, 32266-75

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25271166

Abstract
Here we show how a sperm-specific potassium channel (SLO3) controls Ca(2+) entry into sperm through a sperm-specific Ca(2+) channel, CATSPER, in a totally unanticipated manner. The genetic deletion of either of those channels confers male infertility in mice. During sperm capacitation SLO3 hyperpolarizes the sperm, whereas CATSPER allows Ca(2+) entry. These two channels may be functionally connected, but it had not been demonstrated that SLO3-dependent hyperpolarization is required for Ca(2+) entry through CATSPER channels, nor has a functional mechanism linking the two channels been shown. In this study we show that Ca(2+) entry through CATSPER channels is deficient in Slo3 mutant sperm lacking hyperpolarization; we also present evidence supporting the hypothesis that SLO3 channels activate CATSPER channels indirectly by promoting a rise in intracellular pH through a voltage-dependent mechanism. This mechanism may work through a Na(+)/H(+) exchanger (sNHE) and/or a bicarbonate transporter, which utilizes the inward driving force of the Na(+) gradient, rendering it intrinsically voltage-dependent. In addition, the sperm-specific Na(+)/H(+) exchanger (sNHE) possess a putative voltage sensor that might be activated by membrane hyperpolarization, thus increasing the voltage sensitivity of internal alkalization.