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Requirements of myocyte‐specific enhancer factor 2A in zebrafish cardiac contractility
Author(s) -
Wang Yue-Xiang,
Qian Lin-Xi,
Yu Zhang,
Jiang Qiu,
Dong Yong-Xin,
Liu Xue-Fei,
Yang Xin-Ying,
Zhong Tao P.,
Song Hou-Yan
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2005.07.068
Subject(s) - zebrafish , contractility , sarcomere , cardiac myocyte , myocyte , biology , microbiology and biotechnology , enhancer , morpholino , gene , gene expression , genetics , endocrinology
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.