ZFIN ID: ZDB-PUB-050823-2
Requirements of myocyte-specific enhancer factor 2A in zebrafish cardiac contractility
Wang, Y.X., Qian, L.X., Yu, Z., Jiang, Q., Dong, Y.X., Liu, X.F., Xin-Ying, Y., Zhong, T.P., and Song, H.Y.
Date: 2005
Source: FEBS letters   579(21): 4843-4850 (Journal)
Registered Authors: Song, Houyan, Wang, Yuexiang
Keywords: MEF2A, Cardiac contractility, Zebrafish, Development, Morpholino, Morphant
MeSH Terms:
  • Animals
  • DNA-Binding Proteins/genetics
  • DNA-Binding Proteins/metabolism*
  • Gene Expression
  • Humans
  • MADS Domain Proteins
  • MEF2 Transcription Factors
  • Microinjections
  • Morphogenesis
  • Myocardial Contraction/physiology*
  • Myocardium/metabolism*
  • Myocardium/ultrastructure
  • Myogenic Regulatory Factors
  • Oligonucleotides, Antisense
  • Phenotype
  • Promoter Regions, Genetic
  • RNA Splicing
  • Recombinant Fusion Proteins/genetics
  • Recombinant Fusion Proteins/metabolism
  • Transcription Factors/genetics
  • Transcription Factors/metabolism*
  • Zebrafish/anatomy & histology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism
PubMed: 16107252 Full text @ FEBS Lett.
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.