Wnt11/Fgfr1b cross-talk modulates the fate of cells in palate development |
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Authors: | Lee Jong-Min Kim Jae-Young Cho Kyoung-Won Lee Min-Jung Cho Sung-Won Kwak Sungwook Cai Jinglei Jung Han-Sung |
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Affiliation: | a Division in Anatomy and Developmental Biology, Department of Oral Biology, Research Center for Orofacial Hard Tissue Regeneration, Brain Korea 21 project, Oral Science Research Center, College of Dentistry, Yonsei Center of Biotechnology, Yonsei University, 134 Shinchon-Dong, Seodaemoon-Gu, Seoul, 120-752, Seoul, Republic of Korea b Department of Biochemistry, School of Dentistry, Kyungpook National University, Seoul, Republic of Korea |
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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. |
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Keywords: | Wnt11 Fgfr1b Palatogenesis Palatal growth Palatal fusion Cell proliferation Apoptosis z-VAD-fmk Wnt11 siRNA |
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