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Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5
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Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

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Induction of Id2 expression by cardiac transcription factors GATA4 and Nkx2.5

Joong-Yeon Lim1, Won Ho Kim, Joon Kim

  • 1Division of Intractable Diseases, Center for Biomedical Sciences, National Institute of Health, 194, Tongillo, Eunpyeong-gu, Seoul 122-701, Korea.

Journal of Cellular Biochemistry
|June 15, 2007
PubMed

Insights

GATA4 and Nkx2.5 transcription factors activate Id2 gene expression during cardiomyocyte differentiation. Id proteins then inhibit GATA4 and Nkx2.5, suggesting a regulatory role in heart development.

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Stem Cell Research

Background:

  • Inhibitor of differentiation/DNA binding (Id) proteins regulate cell differentiation.
  • Id proteins interact with helix-loop-helix proteins in cell lineage commitment.

Purpose of the Study:

  • Investigate the upstream regulatory mechanism of Id2 induction during cardiomyocyte differentiation.
  • Identify transcription factors that control Id2 gene expression.

Main Methods:

  • Bioinformatic analysis of the Id2 promoter region.
  • Electrophoretic mobility shift assays (EMSA) to identify transcription factor binding sites.
  • Reporter gene assays with Id2 promoter deletion and mutation constructs.
  • Overexpression studies of GATA4 and Nkx2.5.

Main Results:

  • GATA4 and Nkx2.5 bind to specific sites on the Id2 promoter.
  • Two key motifs (-497/-502 and -264/-270) are crucial for Id2 promoter activation.
  • Overexpression of GATA4 and/or Nkx2.5 increases Id2 promoter activity and protein levels.
  • Id proteins inhibit GATA4 and Nkx2.5-mediated transcription.

Conclusions:

  • GATA4 and Nkx2.5 are identified as upstream regulators of Id2 expression.
  • Id proteins may play a feedback regulatory role in cardiogenesis.

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