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

Aging Fibroblast Growth Factor Maxilla - Cytology - Growth & Development z-VAD-fmk Apoptosis Polymerase Chain Reaction Small Interfering - Genetics Aging - Physiology Mice Palate/growth & development Receptor, Fibroblast Growth Factor, Type 1 - Genetics - Physiology Maxilla Wnt Proteins/physiology* RNA, Small Interfering Cell proliferation In Situ Hybridization Mice, Inbred Icr Mice, Inbred ICR 0303 health sciences Palatal fusion Wnt11 siRNA Inbred ICR Inbred Icr Immunohistochemistry Electroporation Palatogenesis Small Interfering/genetics Wnt Proteins - Genetics - Physiology Maxilla/growth & development Receptor Wnt11 570 Maxilla/cytology 610 03 medical and health sciences Organ Culture Techniques Type 1/physiology* 616 Animals Receptor, Fibroblast Growth Factor, Type 1 Molecular Biology Wnt Proteins/genetics Fgfr1b Palate - Cytology - Growth & Development Palate Type 1 - Genetics - Physiology Receptor Cross-Talk/physiology Cell Biology Receptor Cross-Talk Aging/physiology Palatal growth Wnt Proteins Palate/cytology* Receptor Cross-Talk - Physiology Rna, Small Interfering - Genetics RNA Rna Type 1/genetics Developmental Biology
DOI: 10.1016/j.ydbio.2007.11.033 Publication Date: 2008-01-12T12:20:42Z
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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