The present report tested the hypothesis that focal adhesion kinase (FAK) is a myocellular transducer of mechanical signals towards downstream transcript expression of protein turnover and oxidative metabolism in myofibres. This was approached in an integrative setting combining somatic transgenesis with high-throughput transcript profiling and morphometry in a physiological model for load-dependent atrophy and hypertrophy of anti-gravitational soleus muscle. Focal adhesion signalling in myofibres was perturbed via targeted overexpression of FAK and its inhibitor FRNK (FAK-related non-kinase) in soleus muscle fibres. Experimental bias was supervised by quantitative assessment of transcript level changes versus non-transfected or empty-transfected paired controls. The results points out that sarcolemmal and sarcoplasmic FAK pools separately control gene ontologies underlying load-dependent growth and differentiation of muscle fibres towards a fatigue-resistant phenotype. These findings expose FAK as a key upstream element of the mechano-dependent control of the slow oxidative muscle phenotype and highlight the resolution power of the outlined setting for system biological investigations in vivo.
Life Sciences 2007 (2007) Proc Life Sciences, C57
Research Symposium: Focal adhesion kinase controls load-dependent transcript expression in slow oxidative rat muscle
M. Flueck2, 1, A. Durieux2, D. Desplanches3, D. Freyssenet4
1. Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Alsager, United Kingdom. 2. Institute of Anatomy, University of Berne, Bern , Switzerland. 3. Laboratory of Integrative, Cellular and Molecular Physiology, University of Lyon, Lyon, France. 4. Laboratory of Physiology and Physiopathology of Exercise and Handicap, University of Saint Etienne, Saitn Etienne, France.
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Where applicable, experiments conform with Society ethical requirements.