Journal
GENES & DEVELOPMENT
Volume 15, Issue 12, Pages 1493-1505Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.892301
Keywords
sox; gut endoderm; Nodal; bonnie and clyde; faust; casanova
Categories
Funding
- NIDDK NIH HHS [R01 DK058181, DK58181] Funding Source: Medline
Ask authors/readers for more resources
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 eas 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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available