Hox and Cdx genes are phylogenetically related transcription factor-encoding genes that control positional tissue identity during embryonic develop- ment. In addition, mutations impairing Cdx activity in mice elicit poste- rior body truncations, affecting the axial skeleton, the neuraxis and cau- dal uro-rectal structures. This phenotype of precocious axial termination has not been reported for Hox loss of function mutations. We show that trunk Hox genes stimulate axial extension as they are able to largely rescue the caudal truncations seen in Cdx loss of function embryos. Paralogous group 13 Hox genes on the contrary cause premature arrest of posterior axial growth when precociously expressed. Our data suggest that the time-related shift between expression of trunk and posterior Hox genes successively regulates construction and termination of axial structures in the mouse embryo. Thus, Hox genes seem to differentially orchestrate the complex process of posterior expansion of embryonic tissues during axial morphogenesis as an integrated part of their function in specifying head to tail identity. In addition, we present evidence for a mechanism whereby the Cdx and Hox transcription factors exert their axial extension control by differentially maintaining Wnt signaling in the posterior region during trunk and tail elongation. Moreover, these transcription factors protect the posterior growth zone from retinoic acid during trunk elongation by stimulating Cyp26a1 expression, until they are down regulated past the trunk-tail transition
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