casanova encodes a novel Sox-related protein necessary and sufficient for early endoderm formation in zebrafish

  1. Yutaka Kikuchi1,4,
  2. Antoine Agathon2,4,
  3. Jonathan Alexander1,
  4. Christine Thisse2,
  5. Steven Waldron1,
  6. Deborah Yelon1,3,
  7. Bernard Thisse2, and
  8. Didier Y.R. Stainier1,5
  1. 1Department of Biochemistry and Biophysics, Programs in Genetics, Human Genetics, and Developmental Biology, University of California, San Francisco, California 94143-0448, USA; 2Institut de Génétique et Biologie Moléculaire et Cellulaire CNRS/INSERM/ULP, BP 163, 67404 Illkirch cedex, CU de Strasbourg, France

Abstract

Early endoderm formation in zebrafish requires at least three loci that function downstream of Nodal signaling but upstream of the early endodermal marker sox17: bonnie and clyde (bon), faust (fau), and casanova (cas). cas mutants show the most severe phenotype as they do not form any gut tissue and lack all sox17 expression. Activation of the Nodal signaling pathway or overexpression of Bon or Fau/Gata5 fails to restore anysox17 expression in cas mutants, demonstrating thatcas plays a central role in endoderm formation. Here we show that cas encodes a novel member of the Sox family of transcription factors. Initial cas expression appears in the dorsal yolk syncytial layer (YSL) in the early blastula, and is independent of Nodal signaling. In contrast, endodermal expression ofcas, which begins in the late blastula, is regulated by Nodal signaling. Cas is a potent inducer of sox17 expression in wild-type embryos as well as in bon and fau/gata5mutants. Cas is also a potent inducer of sox17 expression inMZoep mutants, which cannot respond to Nodal signaling. In addition, ectopic expression of cas in presumptive mesodermal cells leads to their transfating into endoderm. Altogether, these data indicate that Cas is the principal transcriptional effector of Nodal signaling during zebrafish endoderm formation.

Keywords

Footnotes

  • 3 Present address: Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA.

  • 4 These authors contributed equally to this work.

  • 5 Corresponding author.

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

  • Article and publication are at www.genesdev.org/cgi/doi/10.1101/gad.892301.

    • Received February 28, 2001.
    • Accepted April 13, 2001.
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