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The SLO3 sperm‐specific potassium channel plays a vital role in male fertility
Author(s) -
Santi Celia M.,
Martínez-López Pablo,
de la Vega-Beltrán José Luis,
Butler Alice,
Alisio Arturo,
Darszon Alberto,
Salkoff Lawrence
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.02.005
Subject(s) - capacitation , hyperpolarization (physics) , depolarization , sperm , potassium channel , membrane potential , acrosome reaction , acrosome , microbiology and biotechnology , sperm motility , motility , biophysics , mutant , chemistry , biology , biochemistry , genetics , organic chemistry , nuclear magnetic resonance spectroscopy , gene
Here we show a unique example of male infertility conferred by a gene knockout of the sperm‐specific, pH‐dependent SLO3 potassium channel. In striking contrast to wild‐type sperm which undergo membrane hyperpolarization during capacitation, we found that SLO3 mutant sperm undergo membrane depolarization. Several defects in SLO3 mutant sperm are evident under capacitating conditions, including impaired motility, a bent “hairpin” shape, and failure to undergo the acrosome reaction (AR). The failure of AR is rescued by valinomycin which hyperpolarizes mutant sperm. Thus SLO3 is the principal potassium channel responsible for capacitation‐induced hyperpolarization, and membrane hyperpolarization is crucial to the AR.