Control of Mouse Cardiac Morphogenesis and Myogenesis by Transcription Factor MEF2C

  • Qing Lin
    Q. Lin and E. N. Olson, Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235–9148, USA.
  • John Schwarz
    Q. Lin and E. N. Olson, Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235–9148, USA.
  • Corazon Bucana
    Q. Lin and E. N. Olson, Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235–9148, USA.
  • Eric N. Olson
    Q. Lin and E. N. Olson, Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235–9148, USA.

抄録

<jats:p> Members of the myocyte enhancer factor–2 (MEF2) family of MADS (MCM1, agamous, deficiens, serum response factor)–box transcription factors bind an A-T–rich DNA sequence associated with muscle-specific genes. The murine <jats:italic>MEF2C</jats:italic> gene is expressed in heart precursor cells before formation of the linear heart tube. In mice homozygous for a null mutation of <jats:italic>MEF2C</jats:italic> , the heart tube did not undergo looping morphogenesis, the future right ventricle did not form, and a subset of cardiac muscle genes was not expressed. The absence of the right ventricular region of the mutant heart correlated with down-regulation of the <jats:italic>dHAND</jats:italic> gene, which encodes a basic helix-loop-helix transcription factor required for cardiac morphogenesis. Thus, MEF2C is an essential regulator of cardiac myogenesis and right ventricular development. </jats:p>

収録刊行物

  • Science

    Science 276 (5317), 1404-1407, 1997-05-30

    American Association for the Advancement of Science (AAAS)

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