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Vol. 15, No. 12, pp. 1493-1505, June 15, 2001
1 Department of Biochemistry and Biophysics, Programs in
Genetics, Human Genetics, and Developmental Biology, University of
California, San Francisco, California 94143-0448, USA;
2 Institut de Génétique et Biologie Moléculaire et
Cellulaire CNRS/INSERM/ULP, BP 163, 67404 Illkirch cedex, CU de
Strasbourg, France
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 any
sox17 expression in cas mutants, demonstrating that
cas 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 of
cas, 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/gata5
mutants. Cas is also a potent inducer of sox17 expression in
MZoep 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.
[Key Words: Sox; gut endoderm; Nodal; bonnie and clyde; faust; casanova]
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