β-catenin/cyclin D1 mediated development of suture mesenchyme in calvarial morphogenesis.

ABSTRACT:

Background

Mouse genetic study has demonstrated that Axin2 is essential for calvarial development and disease. Haploid deficiency of β-catenin alleviates the calvarial phenotype caused by Axin2 deficiency. This loss-of-function study provides evidence for the requirement of β-catenin in exerting the downstream effects of Axin2.

Results

Here we utilize a gain-of-function analysis to further assess the role of β-catenin. A transgenic expression system permitting conditional activation of β-catenin in a spatiotemporal specific manner has been developed. Aberrant stimulation of β-catenin leads to increases in expansion of skeletogenic precursors and the enhancement of bone ossification reminiscent to the loss of Axin2. The constitutively active signal promotes specification of o

SUBMITTER: Mirando AJ 

PROVIDER: S-EPMC3001432 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature