Inhibition of mesodermal fate by Xenopus HNF3β/FoxA2

The winged-helix transcription factor HNF3β/FoxA2 is expressed in embryonic organizing centers of the gastrulating mouse, frog, fish, and chick. In the mouse, HNF3β is required for the formation of the mammalian node and notochord, and can induce ectopic floor plate formation when misexpressed in th...

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Bibliographic Details
Published inDevelopmental biology Vol. 265; no. 1; pp. 90 - 104
Main Authors Suri, Crystal, Haremaki, Tomomi, Weinstein, Daniel C
Format Journal Article
LanguageEnglish
Published Elsevier Inc 2004
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Summary:The winged-helix transcription factor HNF3β/FoxA2 is expressed in embryonic organizing centers of the gastrulating mouse, frog, fish, and chick. In the mouse, HNF3β is required for the formation of the mammalian node and notochord, and can induce ectopic floor plate formation when misexpressed in the developing neural tube; HNF3β expression in the extraembryonic endoderm is also necessary for the proper morphogenesis of the mammalian primitive streak. In the frog Xenopus laevis, several lines of evidence suggest that the related winged-helix factor Pintallavis functions as the ortholog of mammalian HNF3β in both axial mesoderm and neurectoderm; the role of Xenopus HNF3β itself, however, has not been clearly defined, and is the subject of this study. HNF3β is widely expressed in the vegetal pole but, as previously suggested, is excluded from the gastrula-stage mesoderm. We find that expression of an HNF3β-Engrailed repressor fusion protein induces ectopic axes and inhibits head formation in Xenopus embryos, while ectopic HNF3β inhibits mesoderm and anterior endoderm formation in explant assays and in vivo. Our studies suggest that HNF3β target genes function to limit the extent of mesoderm formation in the Xenopus gastrula, and point to related roles for Xenopus HNF3β and the extraembryonic component of mammalian HNF3β during vertebrate gastrulation.
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These authors contributed equally to this work
Graduate training program in Mechanisms of Disease and Therapy
ISSN:0012-1606
1095-564X
DOI:10.1016/j.ydbio.2003.09.017