Submitted on January 17, 2006
Accepted on January 31, 2006
Foxl1-deficient mice exhibit aberrant epithelial cell positioning due to dysregulated EphB/EphrinB expression in the small intestine
Masumi Takano-Maruyama1, Koji Hase1, Hiroshi Fukamachi1, Yasutaka Kato1, Haruhiko Koseki1, and Hiroshi Ohno1*
1 Laboratory for Epithelial Immunobiology, Research Center for Allergy and Immunology, Yokohama, Kanagawa, Japan
* To whom correspondence should be addressed. E-mail: ohno{at}rcai.riken.jp.
The winged helix transcription factor Foxl1 expressed in the gut mesenchyme
regulates epithelial cell proliferation and differentiation through the Wnt/
-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 the 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/-catenin pathway and the subsequent EphB/EphrinB expression.
