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First published online 15 December 2004
doi: 10.1242/jcs.01584

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Absence of Dp71 in mdx^3cv mouse spermatozoa alters flagellar morphology and the distribution of ion channels and nNOS

¹ Departamento de Biología Celular y, CINVESTAV. Apdo. postal 14740, 07000 México, D.F., México
² INSERM U-128. Groupe Muscles et Pathologies, Institut Bousson-Bertrand, 778 rue de la Croix Verte, 34196 Montpellier CEDEX 5, France
³ INSERM U-592, Lab. de Physiopathologie Cellulaire et Moléculaire de la Rétine, Hôpital Saint-Antoine, 184 rue du Faubourg Saint-Antoine, 75571 Paris CEDEX 5, France
⁴ Departamento de Fisiología, Biofísica y Neurociencias, CINVESTAV. Apdo. postal 14740, 07000 México, D.F., México

^* Author for correspondence (e-mail: eoton{at}cell.cinvestav.mx)

Accepted 7 October 2004

In muscle, the absence of dystrophin alters the dystrophin-associated protein complex (DAPC), which is involved in the clustering and anchoring of signaling proteins and ion and water channels. Here we show that mice spermatozoa express only dystrophin Dp71 and utrophin Up71. The purpose of this study was to explore the effect of the absence of Dp71 on the morphology and membrane distribution of members of the DAPC, ion channels and signaling proteins of spermatozoa obtained from dystrophic mutant mdx^3cv mice. Our work indicates that although the absence of Dp71 results in a dramatic decrease in ß-dystroglycan, it induces membrane redistribution and an increase in the total level of -syntrophin, voltage-dependent Na⁺ (µ1) and K⁺ (Kv1.1) channels and neural nitric oxide synthase (nNOS). The short utrophin (Up71) was upregulated and redistributed in the spermatozoa of mdx^3cv mice. A significant increase in abnormal flagella morphology was observed in the absence of Dp71, which was partially corrected when the plasma membrane was eliminated by detergent treatment. Our observations point to a new phenotype associated with the absence of Dp71. Abnormal flagellar structure and altered distribution of ion channels and signaling proteins may be responsible for the fertility problems of mdx^3cv mice.

Key words: Duchenne muscular dystrophy, Cytoskeleton, Motility, Syntrophin-associated proteins, Utrophin upregulation

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