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Acta Physiologica 2011; Volume 202, Supplement 685
Scandinavian Physiological Society's Annual Meeting
8/12/2011-8/14/2011
Bergen, Norway
MYOSIN BINDING PROTEIN C (MYBPC) PLAYS A ROLE IN CONTRACTION OF ZEBRAFISH SKELETAL MUSCLE
Abstract number: 8.1.34
LI1 M, ANDERSSON-LENDAHL1 M, ARNER1 A
1Department of Physiology and Pharmacology, Karolinska Insitutet, Sweden; Email: [email protected]
Aims:
Myosin binding protein C is a thick filament associated protein in muscle with several tissue-specific subtypes: cardiac type, skeletal fast type and skeletal slow type. The encoding genes are highly conserved within vertebrates. Alterations in the cardiac type have been linked to human heart diseases, e.g., familial hypertrophic cardiomyopathy. However, the functions of the skeletal types remain poorly understood. We have established a zebrafish model for muscle physiology (Dou et al., J Gen Physiol, 2008) and present here functional data of the MyBPC fast type in skeletal muscle.
Methods:
The expression pattern of the MyB PC gene in zebrafish larvae was examined by RT-PCR. Morpholino antisense oligonuceotides were injected in fertilized eggs to knock down gene expression, and protein products were later examined by silver staining. Fish muscles were mounted for mechanical measurements during the larval stage (47 dpf).
Results:
The fast skeletal type (MyBPC-2b) was dominantly expressed in zebrafish somites, and could be knocked down with morpholino antisense oligonucleotides by about 50% percent. The developmental process and morphology of skeletal muscle were not significantly affected by knock-down. However, the maximal force generation was impaired in morphant fish larvae, in comparison with control groups. In addition, the morphant muscles exhibited a tendency to fatigue when stimulated with high frequency electrical pulses.
Conclusion:
MyBPC fast type is abundantly expressed and is crucial for the contraction of zebrafish skeletal muscle.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 685 :8.1.34