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Calmodulin and CaMKII in the Sperm Principal Piece: Evidence for a Motility-Related Calcium/Calmodulin Pathway

MARCELA A. MICHAUT

JOHN L. MCELWEE

COLLIN A. WOLFF

ALEXANDER J. TRAVIS

From the ^* Center for Animal Transgenesis and Germ Cell Research, Department of Clinical Studies, University of Pennsylvania New Bolton Center, Kennett Square, Pennsylvania; Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania; and The James A. Baker Institute for Animal Health, College of Veterinary Medicine, Cornell University, Ithaca, New York.

Correspondence to: Regina M Turner, New Bolton Center, University of Pennsylvania School of Veterinary Medicine, 382 West Street Rd, Kennett Square, PA 19348 (e-mail: rmturner{at}vet.upenn.edu).

Both cyclic AMP (cAMP)/protein kinase A (PKA) and calcium (Ca²⁺) signaling pathways are known to be involved in the regulation of motility in mammalian sperm. Calmodulin (CaM) is a ubiquitous Ca²⁺ sensor that has been implicated in the acrosome reaction. In this report, we identify an insoluble pool of CaM in sperm and show that the protein, in addition to its presence in the acrosome, is found in the principal piece of the flagellum. These findings are consistent with, though not proof of, the presence of a pool of CaM in the fibrous sheath. The Ca²⁺/CaM-dependent protein kinase IIß (CaMKIIß), which is a downstream target of Ca²⁺/CaM, similarly localizes to the principal piece. In addition, we confirm earlier reports that a CaM inhibitor decreases sperm motility. However, we find that this inhibition can be largely reversed by stimulation of PKA if substrates for oxidative respiration are present in the medium. Our results suggest that the Ca²⁺/CaM/CaMKII signaling pathway in the sperm principal piece is involved in regulating sperm motility, and that this pathway functions either in parallel with or upstream of the cAMP/PKA pathway.

     Key words: Motility, flagellum

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