1. Howard Hughes Medical Institute, Department of Cardiology, Children's Hospital and Department of Neurobiology, Harvard Medical School Enders 1309, Children's Hospital Boston 320 Longwood Avenue, Boston, Massachusetts 02115, USA

Correspondence to: David E. Clapham¹ Correspondence and requests for materials should be addressed to D.E.C. (dclapham@enders.tch.harvard.edu).

Abstract

In mammals, sperm cells become motile during ejaculation and swim up the female reproductive tract. Before fertilization and to overcome various barriers, their motility must be hyperactivated, a motion that is characterized by vigorous asymmetric tail beating¹. Hyperactivation requires an increase in calcium in the flagella, a process that probably involves plasmalemmal ion channels^{2, 3, 4, 5, 6, 7, 8}. Numerous attempts in the past two decades to understand sperm cell channels have been frustrated by the difficulty of measuring spermatozoan transmembrane ion currents^{2, 3, 9, 10, 11, 12, 13, 14, 15, 16}. Here, by using a simple approach to patch-clamp spermatozoa and to characterize whole-spermatozoan currents, we describe a constitutively active flagellar calcium channel that is strongly potentiated by intracellular alkalinization. This current is not present in spermatozoa lacking the sperm-specific putative ion channel protein, CatSper1. This plasma membrane protein of the six transmembrane-spanning ion channel superfamily is specifically localized to the principal piece of the sperm tail and is required for sperm cell hyperactivation and male fertility^{4, 5}. Our results identify CatSper1 as a component of the key flagellar calcium channel, and suggest that intracellular alkalinization potentiates CatSper current to increase intraflagellar calcium and induce sperm hyperactivation.

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