Requirements of myocyte‐specific enhancer factor 2A in zebrafish cardiac contractility
Yuexiang Wang, Linxi Qian, Yu Zhang, Jiang Qiu, Yongxin Dong, Xuefei Liu, Xinying Yang, Tao P. Zhong, Houyan Song
Abstract
Yuexiang Wang, Linxi Qian, Yu Zhang, Jiang Qiu, Yongxin Dong, Xuefei Liu, Xinying Yang, Tao P. Zhong, Houyan Song
Abstract
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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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.
Key concepts: Zebrafish, Contractility, Sarcomere, Cardiac myocyte, Myocyte, Biology, Cell biology, Enhancer