Zequn Tang

TL;DR: It is demonstrated that Msx2 is essential at multiple sites during organogenesis, including in the axial and appendicular skeleton, and post-natal deficits in Pth/PthRp receptor (Pthr) signalling and in expression of marker genes for bone differentiation indicate that MsX2 is required for both chondrogenesis and osteogenesis.

TL;DR: A model of osteoblast differentiation integrating Twist and FGF in the same pathway, in which FGF acts both at early and late stages is proposed, which may lead to craniosynostosis.

TL;DR: It is suggested that PFM and craniosynostosis result, respectively, from loss and gain of activity in an MSX2-mediated pathway of calvarial osteogenic differentiation.

TL;DR: It is shown that general overexpression of Msx2 under the control of the broadly expressed CMV promoter causes the calvarial bones to invade the sagittal suture, and that an important early event in MSX2-mediated craniosynostosis in humans is a transient retardation of osteogenic cell differentiation in the suture and a consequent increase in the pool of osteogenesis cells.

TL;DR: DNA binding studies show that the craniosynostosis and parietal foramina arise from gain and loss of function, respectively, which suggests a common pathological mechanism, whereby enhanced affinity for a limited repertoire of tissue-specific ligand(s) excessively prolongs signalling in the cranial suture.