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By David P Rice

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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. Tgf␤2 has a role in promoting suture fusion while Tgf␤3 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.

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