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CATSPER Channel-Mediated Ca²⁺ Entry into Mouse Sperm Triggers a Tail-to-Head Propagation¹

Department of Biology³ and Department of Physiology,⁴ University of Pennsylvania, Philadelphia, Pennsylvania 19104

ABSTRACT

Many Ca²⁺ channel proteins have been detected in mammalian sperm, but only the four CATSPER channels have been clearly shown to be required for male fertility. Ca²⁺ entry through the principal piece-localized CATSPER channels has been implicated in the activation of hyperactivated motility. In the present study, we show that the Ca²⁺ entry also triggers a tail-to-head Ca²⁺ propagation in the mouse sperm. When activated with 8-Br-cAMP, 8-Br-cGMP, or alkaline depolarization, a CATSPER-dependent increase in intracellular Ca²⁺ concentration starts in the principal piece, propagates through the midpiece, and reaches the head in a few seconds. The Ca²⁺ propagation through the midpiece leads to a Ca²⁺-dependent increase in NADH fluorescence. In addition, CatSper1-mutant sperm have lower intracellular ATP levels than wild-type sperm. Thus, a Ca²⁺ influx in the principal piece through CATSPER channels can not only initiate hyperactivated motility, but can also trigger a tail-to-head Ca²⁺ propagation that leads to an increase in [NADH] and may regulate ATP homeostasis.

acrosome reaction, calcium, sperm capacitation, sperm motility and transport

¹Supported by NIH grants 1R01HD047578, 1R03HD045290, and 1R01EY013434 and the University of Pennsylvania Research Foundation.

Correspondence: ²Dejian Ren, Department of Biology, University of Pennsylvania, 415 South University Ave., Philadelphia, PA 19104. FAX: 215 898 8780; e-mail: dren{at}sas.upenn.edu

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