J. Cell Biol., Volume 142, Number 6, September 21, 1998 1461-1471

Progressive Muscular Dystrophy in -Sarcoglycan-deficient Mice

Franck Duclos,^* Volker Straub,^* Steven A. Moore, David P. Venzke,^* Ron F. Hrstka,^§ Rachelle H. Crosbie,^* Madeleine Durbeej,^* Connie S. Lebakken,^* Audrey J. Ettinger, Jack van der Meulen,^** Kathleen H. Holt,^* Leland E. Lim,^* Joshua R. Sanes, Beverly L. Davidson,^¶ John A. Faulkner,^** Roger Williamson,^§ and Kevin P. Campbell^*

^* Howard Hughes Medical Institute, Department of Physiology and Biophysics and Department of Neurology, University of Iowa College of Medicine, Iowa City, Iowa 52242-1101;  Department of Pathology and ^§ Department of Obstetrics and Gynecology, University of Iowa College of Medicine, Iowa City, Iowa 52242;   Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110; ^¶ Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa 52242; and ^** Institute of Gerontology, University of Michigan, Ann Arbor, Michigan 48109

Limb-girdle muscular dystrophy type 2D (LGMD 2D) is an autosomal recessive disorder caused by mutations in the -sarcoglycan gene. To determine how -sarcoglycan deficiency leads to muscle fiber degeneration, we generated and analyzed -sarcoglycan- deficient mice. Sgca-null mice developed progressive muscular dystrophy and, in contrast to other animal models for muscular dystrophy, showed ongoing muscle necrosis with age, a hallmark of the human disease. Sgca-null mice also revealed loss of sarcolemmal integrity, elevated serum levels of muscle enzymes, increased muscle masses, and changes in the generation of absolute force. Molecular analysis of Sgca-null mice demonstrated that the absence of -sarcoglycan resulted in the complete loss of the sarcoglycan complex, sarcospan, and a disruption of -dystroglycan association with membranes. In contrast, no change in the expression of -sarcoglycan (-sarcoglycan homologue) was observed. Recombinant -sarcoglycan adenovirus injection into Sgca-deficient muscles restored the sarcoglycan complex and sarcospan to the membrane. We propose that the sarcoglycan-sarcospan complex is requisite for stable association of -dystroglycan with the sarcolemma. The Sgca-deficient mice will be a valuable model for elucidating the pathogenesis of sarcoglycan deficient limb-girdle muscular dystrophies and for the development of therapeutic strategies for this disease.

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