![]() ![]() Received: JAccepted: FebruPublished: February 17, 2016Ĭopyright: © 2016 Szabo-Rogers et al. PLoS ONE 11(2):Įditor: Andre van Wijnen, University of Massachusetts Medical, UNITED STATES Taken together, our work defines a novel role for Gsk3β in skull development.Ĭitation: Szabo-Rogers H, Yakob W, Liu KJ (2016) Frontal Bone Insufficiency in Gsk3β Mutant Mice. This phenotype appears to be Wnt-independent and is not rescued by decreasing the genetic dose of β-catenin/Ctnnb1. ![]() This leads to a smaller condensation and premature differentiation. In the absence of Gsk3β the frontal bone primordium undergoes increased cell death and reduced proliferation with a concomitant increase in Fgfr2-IIIc and Twist1 expression. In this report, we find that loss of Gsk3β leads to a fully penetrant reduction of frontal bone size and subsequent enlarged frontal fontanelle. For example, insufficient ossification of the bony elements leads to enlarged anterior fontanelles and reduced mechanical protection of the brain. Disrupting this balance can lead to changes in the shape and size of skull bones, which can have serious clinical implications. The development of the mammalian skull is a complex process that requires multiple tissue interactions and a balance of growth and differentiation.
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