Among several candidate Ca 2+ entry channels in sperm, only CatSper1 and CatSper2 are
known to have required roles in male fertility. Past work with CatSper1 null sperm indicates
that a critical lesion in hyperactivated motility underlies the infertility phenotype and is
associated with an absence of depolarization-evoked Ca 2+ entry. Here we show that failure
of hyperactivation of CatSper2 null sperm similarly correlates with an absence of
depolarization evoked Ca 2+ entry. Additional shared aspects of the phenotypes of …