A novel gene required for male fertility and functional CATSPER channel formation in spermatozoa

Jean-Ju Chung, Betsy Navarro, Grigory Krapivinsky, Luba Krapivinsky and David E. Clapham ()
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Jean-Ju Chung: Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital
Betsy Navarro: Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital
Grigory Krapivinsky: Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital
Luba Krapivinsky: Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital
David E. Clapham: Howard Hughes Medical Institute, Manton Center for Orphan Disease, Children's Hospital

Nature Communications, 2011, vol. 2, issue 1, 1-12

Abstract: Abstract Calcium signalling is critical for successful fertilization. In spermatozoa, capacitation, hyperactivation of motility and the acrosome reaction are all mediated by increases in intracellular Ca2+. Cation channels of sperm proteins (CATSPERS1–4) form an alkalinization-activated Ca2+-selective channel required for the hyperactivated motility of spermatozoa and male fertility. Each of the CatSper1–4 genes encodes a subunit of a tetramer surrounding a Ca2+-selective pore, in analogy with other six-transmembrane ion channel α subunits. In addition to the pore-forming proteins, the sperm Ca2+ channel contains auxiliary subunits, CATSPERβ and CATSPERγ. Here, we identify the Tmem146 gene product as a novel subunit, CATSPERδ, required for CATSPER channel function. We find that mice lacking the sperm tail-specific CATSPERδ are infertile and their spermatozoa lack both Ca2+ current and hyperactivated motility. We show that CATSPERδ is an essential element of the CATSPER channel complex and propose that CATSPERδ is required for proper CATSPER channel assembly and/or transport.

Date: 2011
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DOI: 10.1038/ncomms1153

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