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Am J Physiol Gastrointest Liver Physiol 291: G163-G170, 2006. First published February 9, 2006; doi:10.1152/ajpgi.00019.2006
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MUCOSAL BIOLOGY

Foxl1-deficient mice exhibit aberrant epithelial cell positioning resulting from dysregulated EphB/EphrinB expression in the small intestine

Masumi Takano-Maruyama,1 Koji Hase,1 Hiroshi Fukamachi,2 Yasutaka Kato,3 Haruhiko Koseki,4 and Hiroshi Ohno1,5

1Laboratory for Epithelial Immunobiology and 4Developmental Genetics, Research Center for Allergy and Immunology, RIKEN, Kanagawa; 2Department of Molecular Oncology, Graduate School of Medicine and Dentistry, Tokyo Medical and Dental University, Tokyo; 3Second Department of Internal Medicine, School of Medicine, Chiba University, Chiba; and 5International Graduate School of Arts and Sciences, Yokohama City University, Kanagawa, Japan

Submitted 17 January 2006 ; accepted in final form 31 January 2006

The winged helix transcription factor Foxl1, expressed in the gut mesenchyme, regulates epithelial cell proliferation and differentiation through the Wnt/beta-catenin pathway. To better understand the role of Foxl1 in epithelial morphogenesis, we examined the tissue structure and positioning of epithelial cells in the small intestine of Foxl1-deficient mice. The small intestine of Foxl1-deficient mice manifested aberrant crypt structure, including widely distributed Paneth cells, which coincided with the ectopic and increased expression of EphB2 and EphB3, which are key regulators of epithelial cell positioning. Furthermore, real-time quantitative PCR indicated that a subset of Wnt family genes was highly expressed in the gut mesenchyme of Foxl1-deficient mice compared with that of wild-type mice. Such an increase in Wnt expression was remarkable in the mesenchyme, where the aberrant Paneth cell positioning was observed by in situ hybridization. Foxl1 plays an important role in the maintenance of crypt architecture and epithelial cell positioning through the mesenchymal-epithelial interaction in the small intestine. This interaction is essential for the normal regulation of the Wnt/beta-catenin pathway and the subsequent EphB/EphrinB expression.

Foxl1; EphB/EphrinB; Wnt; mesenchymal-epithelial interaction; gut


Address for reprint requests and other correspondence: H. Ohno, Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, RIKEN, 1-7-22 Suehiro, Tsurumi-ku, Yokohama 230-0045, Japan (e-mail: ohno{at}rcai.riken.jp)






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