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First published online September 30, 2004
doi: 10.1242/10.1242/dev.01396

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New roles for FoxH1 in patterning the early embryo

¹ Division of Developmental Biology, Cincinnati Children's Research Foundation, 3333 Burnet Avenue, Cincinnati, OH 45229, USA
² Biomolecular Medicine Group, Department of Biological Sciences, University of Warwick, Gibbet Hill Road, Coventry CV4 7AL, UK
³ Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA

^* Author for correspondence (e-mail: heabq9{at}chmcc.org)

Accepted 5 August 2004

FoxH1 (Fast1) was first characterized as the transcriptional partner for Smad proteins. Together with Smad2/4, it forms the activin response factor (ARF) that binds to the Mix.2 promoter in Xenopus embryos. Foxh1 is expressed maternally in Xenopus. Depletion of maternal Foxh1 mRNA results in abnormalities of head and dorsal axis formation. We show that FoxH1 is required, together with XTcf3/ß catenin, to activate the zygotic expression of the nodal gene, Xnr3 in a Smad2-independent manner. In contrast, maternal FoxH1 acts as an inhibitor of Xnr5 and 6 transcription, preventing their upregulation on the ventral side of the embryo, by the maternal T-box transcription factor VegT. We conclude that maternal FoxH1 has essential, context-dependent roles in regulating the pattern of zygotic gene expression in the early embryo.

Key words: Foxh1, Fast1, Antisense, Nodal, Xnr5, Xnr6, Xnr3, Xenopus

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