Gata5 is required for the development of the heart and endoderm in zebrafish

  1. Jeremy F. Reiter,
  2. Jonathan Alexander,
  3. Adam Rodaway,
  4. Deborah Yelon,
  5. Roger Patient,
  6. Nigel Holder, and
  7. Didier Y.R. Stainier
  1. Department of Biochemistry and Biophysics, Programs in Human Genetics and Developmental Biology, University of California at San Francisco, San Francisco, California 94143-0448 USA; Developmental Biology Research Centre, The Randall Institute, King's College London, London WC2B 5RL, UK; Department of Anatomy and Developmental Biology, University College London, London WC1E 6BT, UK

Abstract

The mechanisms regulating vertebrate heart and endoderm development have recently become the focus of intense study. Here we present evidence from both loss- and gain-of-function experiments that the zinc finger transcription factor Gata5 is an essential regulator of multiple aspects of heart and endoderm development. We demonstrate that zebrafish Gata5 is encoded by the faust locus. Analysis of faust mutants indicates that early in embryogenesis Gata5 is required for the production of normal numbers of developing myocardial precursors and the expression of normal levels of several myocardial genes including nkx2.5. Later, Gata5 is necessary for the elaboration of ventricular tissue. We further demonstrate that Gata5 is required for the migration of the cardiac primordia to the embryonic midline and for endodermal morphogenesis. Significantly, overexpression of gata5 induces the ectopic expression of several myocardial genes including nkx2.5 and can produce ectopic foci of beating myocardial tissue. Together, these results implicate zebrafish Gata5 in controlling the growth, morphogenesis, and differentiation of the heart and endoderm and indicate that Gata5 regulates the expression of the early myocardial gene nkx2.5.

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Footnotes

  • Deceased.

  • Corresponding author.

  • E-MAIL didier_stainier{at}biochem.ucsf.edu; FAX (415) 476-3892.

    • Received July 22, 1999.
    • Accepted October 5, 1999.
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