| First Author | Goodnough LH | Year | 2012 |
| Journal | Development | Volume | 139 |
| Issue | 23 | Pages | 4428-38 |
| PubMed ID | 23095887 | Mgi Jnum | J:189063 |
| Mgi Id | MGI:5444308 | Doi | 10.1242/dev.081679 |
| Citation | Goodnough LH, et al. (2012) Twist1 mediates repression of chondrogenesis by beta-catenin to promote cranial bone progenitor specification. Development 139(23):4428-38 |
| abstractText | The bones of the mammalian skull vault form through intramembranous ossification. Skull bones ossify directly, in a process regulated by beta-catenin, instead of passing through a cartilage intermediate. We tested whether beta-catenin is necessary for fate selection of intramembranous bone progenitors in the skull. Here, we show in mice that removal of beta-catenin from skull bone progenitors results in the near complete transformation of the skull bones to cartilage, whereas constitutive beta-catenin activation inhibits skull bone fate selection. beta-catenin directly activated Twist1 expression in skull progenitors, conditional Twist1 deletion partially phenocopied the absence of beta-catenin, and Twist1 deletion partially restored bone formation in the presence of constitutive beta-catenin activation. Finally, Twist1 bound robustly to the 3'UTR of Sox9, the central initiator of chondrogenesis, suggesting that Twist1 might directly repress cartilage formation through Sox9. These findings provide insight into how beta-catenin signaling via Twist1 actively suppresses the formation of cartilage and promotes intramembranous ossification in the skull. |
