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Am J Physiol Cell Physiol 277: C965-C973, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 5, C965-C973, November 1999

Loss of Hoxa5 gene function in mice perturbs intestinal maturation

Josée Aubin1, Pierre Chailler2, Daniel Ménard2, and Lucie Jeannotte1

1 Centre de Recherche en Cancérologie de l'Université Laval, Centre Hospitalier Universitaire de Québec, Pavillon de L'Hôtel-Dieu de Québec, Québec G1R 2J6; and 2 Groupe du Conseil de Recherches Médicales du Canada sur le Développement Fonctionnel et la Physiopathologie du Tube Digestif, Département d'Anatomie et de Biologie Cellulaire, Faculté de Médecine, Université de Sherbrooke, Sherbrooke, Québec, Canada J1H 5N4

The Hox gene family of transcription factors constitutes candidate regulators in the molecular cascade of events that governs establishment of normal terminal differentiation along the duodenum to colon axis. One member of this family, Hoxa5, displays a dynamic pattern of expression during gut development. Hoxa5 transcripts are present in midgut mesenchyme at the time of remodeling, supporting a role for this gene in digestive tract specification. To study the role of Hoxa5 in proper intestinal development and maturation, we examined whether Hoxa5 mutant mice exhibit any defect in this process. We report here that even though Hoxa5 is not required for midgut morphogenesis, its loss of function perturbs the acquisition of adult mode of digestion, which normally is temporally coordinated with the process of spontaneous weaning. Impaired maturation of the digestive tract might be related to altered specification of intestinal epithelial cells. Our findings provide evidence that Hoxa5 expression in the gut mesoderm is important for the region-specific differentiation of the adjacent endoderm.

Hox gene expression; intestinal enzymes; gut morphogenesis; regional specification; epithelial-mesenchymal interactions


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