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ZFIN ID: ZDB-PUB-060517-17
Hand2 regulates epithelial formation during myocardial diferentiation
Trinh, L.A., Yelon, D., and Stainier, D.Y.
Date: 2005
Source: Current biology : CB   15(5): 441-446 (Journal)
Registered Authors: Stainier, Didier, Trinh, Le, Yelon, Deborah
Keywords: none
MeSH Terms:
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Differentiation/physiology*
  • Cell Polarity/physiology*
  • DNA-Binding Proteins/metabolism
  • Epithelium/embryology
  • GATA5 Transcription Factor
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Microscopy, Confocal
  • Microscopy, Fluorescence
  • Morphogenesis*
  • Myocytes, Cardiac/physiology*
  • Oligonucleotides, Antisense
  • Transcription Factors/metabolism*
  • Transcription Factors/physiology
  • Zebrafish/embryology*
  • Zebrafish Proteins
PubMed: 15786591 Full text @ Curr. Biol.
Myocardial differentiation is initiated by the activation of terminal-differentiation gene expression within a subset of cells in the anterior lateral plate mesoderm. We have previously shown that shortly after this activation, myocardial cells undergo epithelial maturation [1], suggesting that myocardial differentiation encompasses both molecular and cellular changes. To address the question of how the molecular programs driving myocardial gene expression and the formation of the myocardial epithelium are integrated, we analyzed the role of two essential myocardial terminal-differentiation factors, Hand2 and Gata5, in myocardial epithelia formation. hand2 and gata5 mutants exhibit a much-reduced number of myocardial cells and defects in myocardial gene expression [2,3]. We find that the few myocardial precursors that are present in hand2 mutants do not polarize. In contrast, embryos with reduced Gata5 function exhibit polarized myocardial epithelia despite a similar reduction in myocardial precursor number, indicating that proper cell number is not required for epithelial formation. Taken thogether, these results indicate that Hand2 is uniquely required for myocardial polarization, a previously unappreciated role for this critical transcription factor. Furthermore, these results demonstrate that two independent processes, the polarizaton of myocardial precursors and the allocation of proper cell number, contribute to myocardial development.