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Jumonji represses alpha-cardiac myosin heavy chain expression via inhibiting MEF2 activity

Tae-gyun Kim1, Jooyoung Jung, Matthew R Mysliwiec

  • 1Department of Anatomy and Cardiovascular Research Center, University of Wisconsin Medical School, Madison, WI 53706, USA.

Biochemical and Biophysical Research Communications
|March 2, 2005
PubMed

Insights

Jumonji (JMJ) represses alpha-cardiac myosin heavy chain (alphaMHC) gene expression by inhibiting myocyte enhancer factor 2 (MEF2) activity. This protein-protein interaction is crucial for regulating cardiac gene expression during development and disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Genetics
  • Gene Regulation

Background:

  • Alpha-cardiac myosin heavy chain (alphaMHC) gene expression is vital for heart development and function, decreasing in cardiac myopathy.
  • Jumonji (JMJ) is essential for cardiovascular development and acts as a transcriptional repressor.

Purpose of the Study:

  • To investigate the mechanism by which JMJ regulates alphaMHC expression.
  • To determine the role of JMJ in repressing myocyte enhancer factor 2 (MEF2) activity.

Main Methods:

  • Overexpression of JMJ in primary cardiomyocytes.
  • Analysis of alphaMHC gene expression.
  • Investigation of protein-protein interactions between JMJ and MEF2 isoforms.

Main Results:

  • JMJ overexpression significantly reduced endogenous alphaMHC expression.
  • JMJ repressed the synergistic activation of alphaMHC by MEF2 and thyroid hormone receptor (TR).
  • JMJ directly interacted with MEF2A, inhibiting its transcriptional activity.

Conclusions:

  • JMJ represses alphaMHC expression through direct physical interaction with MEF2A.
  • This interaction mechanism is critical for regulating cardiac gene expression and may be relevant in cardiac disease states.

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