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Published online
doi:10.1083/jcb.200704152
The Journal of Cell Biology, Vol. 178, No. 4, 635-648
The Rockefeller University Press, 0021-9525 $30.00
© Bastide et al.
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Article

Sox9 regulates cell proliferation and is required for Paneth cell differentiation in the intestinal epithelium



Pauline Bastide1, Charbel Darido1, Julie Pannequin1, Ralf Kist2, Sylvie Robine3, Christiane Marty-Double4, Frédéric Bibeau5, Gerd Scherer2, Dominique Joubert1, Frédéric Hollande1, Philippe Blache1, and Philippe Jay1

1 Institut National de la Santé et de la Recherche Médicale, U661, Department of Cellular and Molecular Oncology, Institut de Génomique Fonctionnelle, Centre National de la Recherche Scientifique UMR5203, Université de Montpellier I and Université de Montpellier II, Montpellier, F-34094 Montpellier, Cedex 05, France
2 Institute of Human Genetics and Anthropology, University of Freiburg, D-79106 Freiburg, Germany
3 Morphogenesis and Intracellular Signaling, Institut Curie, Centre National de la Recherche Scientifique, 75248 Paris, Cedex 05, France
4 Service d'Anatomie-Pathologie, Centre Hospitalier Universitaire Carémeau, 30000 Nîmes, France
5 Service d'Anatomie-Pathologie, Centre Régional de Lutte contre le Cancer Val d'Aurelle, 34298 Montpellier, Cedex 05, France

Correspondence to Philippe Jay: philippe.jay{at}igf.cnrs.fr

The HMG-box transcription factor Sox9 is expressed in the intestinal epithelium, specifically, in stem/progenitor cells and in Paneth cells. Sox9 expression requires an active ß-catenin–Tcf complex, the transcriptional effector of the Wnt pathway. This pathway is critical for numerous aspects of the intestinal epithelium physiopathology, but processes that specify the cell response to such multipotential signals still remain to be identified. We inactivated the Sox9 gene in the intestinal epithelium to analyze its physiological function. Sox9 inactivation affected differentiation throughout the intestinal epithelium, with a disappearance of Paneth cells and a decrease of the goblet cell lineage. Additionally, the morphology of the colon epithelium was severely altered. We detected general hyperplasia and local crypt dysplasia in the intestine, and Wnt pathway target genes were up-regulated. These results highlight the central position of Sox9 as both a transcriptional target and a regulator of the Wnt pathway in the regulation of intestinal epithelium homeostasis.

R. Kist's present address is Institute of Human Genetics, International Centre for Life, University of Newcastle, Newcastle upon Tyne, NE1 3BZ, England, UK.


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