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Vol. 15, No. 10, pp. 1257-1271, May 15, 2001
1 Samuel Lunenfeld Research Institute, Mount Sinai
Hospital, Toronto, Ontario, Canada M5G 1X5; 2 Department of
Anatomy and Cell Biology and 3 Department of Medical Genetics,
Medical Sciences Building, University of Toronto, Toronto, Ontario,
Canada M5S 1A8
The node and the anterior visceral endoderm (AVE) are important
organizing centers that pattern the mouse embryo by establishing the
anterior-posterior (A-P), dorsal-ventral (D-V), and left-right (L-R) axes. Activin/nodal signaling through the Smad2 pathway has been
implicated in AVE formation and in morphogenesis of the primitive
streak, the anterior end of which gives rise to the node. The forkhead
DNA-binding protein, FoxH1 (or Fast), functions as a Smad DNA-binding
partner to regulate transcription in response to activin signaling.
Here, we show that deletion of FoxH1 in mice results in
failure to pattern the anterior primitive streak (APS) and form node,
prechordal mesoderm, notochord, and definitive endoderm. In contrast,
formation of the AVE can occur in the absence of FoxH1. The
FoxH1 mutant phenotype is remarkably similar to that of
mice deficient in the forkhead protein Foxa2 (HNF3
), and we show
that Foxa2 expression is dependent on FoxH1
function. These results show that FoxH1 functions in an
activin/nodal-Smad signaling pathway that acts upstream of
Foxa2 and is required specifically for patterning the APS
and node in the mouse.
[Key Words: gastrulation; anterior primitive streak; nodal; Smad; FoxH1]
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