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

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 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.

SUBMITTER: Kikuchi Y

PROVIDER: S-EPMC312713 | biostudies-literature | 2001 Jun

REPOSITORIES: biostudies-literature

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

Kikuchi Y Y Agathon A A Alexander J J Thisse C C Waldron S S Yelon D D Thisse B B Stainier D Y DY

Genes & development 20010601 12

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 ...[more]

PMID: 11410530

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Project description:The B1 SOX transcription factors SOX1/2/3/19 have been implicated in various processes of early embryogenesis. However, their regulatory functions in stages from the blastula to early neurula remain largely unknown, primarily because loss-of-function studies have not been informative to date. In our present study, we systematically knocked down the B1 sox genes in zebrafish. Only the quadruple knockdown of the four B1 sox genes sox2/3/19a/19b resulted in very severe developmental abnormalities, confirming that the B1 sox genes are functionally redundant. We characterized the sox2/3/19a/19b quadruple knockdown embryos in detail by examining the changes in gene expression through in situ hybridization, RT-PCR, and microarray analyses. Importantly, these phenotypic analyses revealed that the B1 SOX proteins regulate the following distinct processes: (1) early dorsoventral patterning by controlling bmp2b/7; (2) gastrulation movements via the regulation of pcdh18a/18b and wnt11, a non-canonical Wnt ligand gene; (3) neural differentiation by regulating the Hes-class bHLH gene her3 and the proneural-class bHLH genes neurog1 (positively) and ascl1a (negatively), and regional transcription factor genes, e.g., hesx1, zic1, and rx3; and (4) neural patterning by regulating signaling pathway genes, cyp26a1 in RA signaling, oep in Nodal signaling, shh, and mdkb. Chromatin immunoprecipitation analysis of the her3, hesx1, neurog1, pcdh18a, and cyp26a1 genes further suggests a direct regulation of these genes by B1 SOX. We also found an interesting overlap between the early phenotypes of the B1 sox quadruple knockdown embryos and the maternal-zygotic spg embryos that are devoid of pou5f1 activity. These findings indicate that the B1 SOX proteins control a wide range of developmental regulators in the early embryo through partnering in part with Pou5f1 and possibly with other factors, and suggest that the B1 sox functions are central to coordinating cell fate specification with patterning and morphogenetic processes occurring in the early embryo.

Dataset Information

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

Publications

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

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