Key result
Knock-down of MEF2A in zebrafish impaired cardiac contractility and resulted in sarcomere assembly defects.
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MEF2A is essential for normal cardiac contractility and sarcomere assembly in a zebrafish model.
Myocyte-specific enhancer factor 2A (MEF2A) regulates a broad range of fundamental cellular processes including cell division, differentiation and death. Here, we tested the hypothesis that MEF2A is required in cardiac contractility employing zebrafish as a model organism. MEF2A is highly expressed in heart as well as somites during zebrafish embryogenesis. Knock-down of MEF2A in zebrafish impaires the cardiac contractility and results in sarcomere assembly defects. Dysregulation of cardiac genes in MEF2A morphants suggests that sarcomere assembly disturbances account for the cardiac contractile deficiency. Our studies suggested that MEF2A is essential in cardiac contractility.
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Wang et al. (2005) studied Cardiac contractility. Knock-down of MEF2A was evaluated on Cardiac contractility and sarcomere assembly. Knock-down of MEF2A in zebrafish impaired cardiac contractility and resulted in sarcomere assembly defects.
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