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Molecular and Cellular Biology, April 2004, p. 3514-3525, Vol. 24, No. 8
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.8.3514-3525.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Muscle Regeneration and Myogenic Differentiation Defects in Mice Lacking TIS7

Santhosh K. Vadivelu,^1, Robert Kurzbauer,² Benjamin Dieplinger,¹ Margit Zweyer,³ Ralf Schafer,³ Anton Wernig,³ Ilja Vietor,^1* and Lukas A. Huber^1*

Institute for Anatomy, Histology, and Embryology, Department of Histology and Molecular Cell Biology, Medical University Innsbruck, A-6020 Innsbruck,¹ Institute of Molecular Pathology, A-1030 Vienna, Austria,² Department of Physiology and Neurophysiology, University of Bonn, D-53111 Bonn, Germany³

Received 12 September 2003/ Returned for modification 14 November 2003/ Accepted 14 January 2004

The tetradecanoyl phorbol acetate-induced sequence 7 gene (tis7) is regulated during cell fate processes and functions as a transcriptional coregulator. Here, we describe the generation and analysis of mice lacking the tis7 gene. Surprisingly, TIS7 knockout mice show no gross histological abnormalities and are fertile. Disruption of the tis7 gene by homologous recombination delayed muscle regeneration and altered the isometric contractile properties of skeletal muscles after muscle crush damage in TIS7^-/- mice. Cultured primary myogenic satellite cells (MSCs) from TIS7^-/- mice displayed marked reductions in differentiation potential and fusion index in a strictly cell-autonomous fashion. Loss of TIS7 caused the down-regulation of muscle-specific genes, such as those for MyoD, myogenin, and laminin-2. Fusion potential in TIS7^-/- MSCs could be rescued by TIS7 expression or laminin supplementation. Therefore, TIS7 is not essential for mouse development but plays a novel regulatory role during adult muscle regeneration.

Present address: Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724.

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