By David P Rice
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Extra info for Craniofacial sutures : development, disease and treatment
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They also showed that a similar targeting of a truncated form of Fgfr1, which blocks Fgf signaling, caused infected PF sutures to stay patent. This elegant study showed that Fgf signaling regulates postnatal suture fate. Differential signaling through Tgf isoforms produced by the dura mater have been shown to control calvarial suture patency. Tgf2 has a role in promoting suture fusion while Tgf3 is required to help keep sutures patent [35]. In humans mutations in TGFb receptors 1 and 2, which are proposed to confer a gain-of-function, cause craniosynostosis [24].
In both humans and mice, loss of function mutations in Msx2 and Alx4 result in similar ‘hole in the head’ phenotypes to those exhibited by Foxc1Ϫ/Ϫ mutant mice [58, 64, 65]. References 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 Miyake T, Cameron AM, Hall BK: Stage-specific onset of condensation and matrix deposition for Meckel’s and other first arch cartilages in inbred C57BL/6 mice. J Craniofac Genet Dev Biol 1996;16:32–47. Hall BK, Miyake T: All for one and one for all: condensations and the initiation of skeletal development.
Birth Defects Res C Embryo Today 2005;75:72–80. Modarresi R, Lafond T, Roman-Blas JA, Danielson KG, Tuan RS, Seghatoleslami MR: N-cadherin mediated distribution of beta-catenin alters MAP kinase and BMP-2 signaling on chondrogenesisrelated gene expression. J Cell Biochem 2005;95:53–63. Hartmann C: A Wnt canon orchestrating osteoblastogenesis. Trends Cell Biol 2006;16:151–158. Luo Y, Kostetskii I, Radice GL: N-cadherin is not essential for limb mesenchymal chondrogenesis. Dev Dyn 2005;232:336–344.