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Wnt11/Fgfr1b cross-talk modulates the fate of cells in palate development.

Research paper by Jong-Min JM Lee, Jae-Young JY Kim, Kyoung-Won KW Cho, Min-Jung MJ Lee, Sung-Won SW Cho, Sungwook S Kwak, Jinglei J Cai, Han-Sung HS Jung

Indexed on: 15 Jan '08Published on: 15 Jan '08Published in: Developmental Biology



Abstract

Various cellular and molecular events underlie the elevation and fusion of the developing palate that occurs during embryonic development. This includes convergent extension, where the medial edge epithelium is intercalated into the midline epithelial seam. We examined the expression patterns of Wnt11 and Fgfr1b - which are believed to be key factors in convergent extension - in mouse palate development. Wnt-11 overexpression and beads soaked in SU5402 (an Fgfr1 inhibitor) were employed in in vitro organ cultures. The results suggested that interactions between Wnt11 and Fgfr1b are important in modulating cellular events such as cell proliferation for growth and apoptosis for fusion. Moreover, the Wnt11 siRNA results showed that Wnt11-induced apoptosis was necessary for palatal fusion. In summary, Fgfr1b induces cell proliferation in the developing palate mesenchyme so that the palate grows and contacts each palatal shelf, with negative feedback of Fgfs triggered by excessive cell proliferation then inhibiting the expression of Fgfr1b and activating the expression of Wnt11 to fuse each palate by activating apoptosis.