Transcriptional profiling of myostatin-knockout mice implicates Wnt signaling in postnatal skeletal muscle growth and hypertrophy Carissa A. Steelman * , Justin C. Recknor † , Dan Nettleton and James M. Reecy * ,1 * Department of Animal Science and † Department of Statistics, Iowa State University, Ames, Iowa, USA 1 Correspondence: 2255 Kildee Hall, Ames, IA 50011-3150, USA. E-mail: jreecy@iastate.edu <h3>SPECIFIC AIMS</h3> The aim of this study was to identify myostatin-responsive genes in skeletal muscle. Elucidation of potential downstream targets of myostatin will increase understanding of the mechanism by which it signals to inhibit skeletal muscle growth. <h3>PRINCIPAL FINDINGS</h3> <h3>1. A large number of gene expression differences were observed between myostatin null and wild-type mice</h3> Pectoralis muscles from Mstn –/– and Mstn +/+ mice at 5 wk of age were analyzed using the Affymetrix Mouse Expression Set 430. After Bonferroni correction, 200 genes were identified as differentially expressed. Allowing for a false discovery rate (FDR) of 0.05, the list was expanded to include 2109 genes. <h3>2. Lack of myostatin affected genes involved in a wide variety of biological processes</h3> Examination of functional annotation by the Expression Analysis Systematic Explorer (EASE) revealed that differentially expressed genes encompassed a range
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