Msx2 deficiency in mice causes pleiotropic defects in bone growth and ectodermal organ formation

By I. Satokata, Liang Ma, H. Ohshima, M. Bei, Ian Woo, K. Nishizawa, T. Maeda, Y. Takano, M. Uchiyama, Shaun Heaney and 4 more. Nature Genetics, 2000

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FGF signaling pathways in endochondral and intramembranous bone development and human genetic disease. (2002, background): “In contrast, haploinsufficiency of Msx2 decreases cell proliferation, delays suture closure, and causes defects in skull ossification in both humans and mice (Dodig et al. 1999; Satokata et al. 2000; Wilkie et al. 2000).”
Regulation of osteoblast differentiation by transcription factors (2006, background): “In Msx1 / Msx2 / mice, cranial bone formation is severely inhibited, indicating that Msx1 and Msx2 have a redundant function in cranial bone formation [Satokata et al., 2000].”
DiGeorge syndrome phenotype in mice mutant for the T-box gene, Tbx1 (2001, background): “In both of those cases, heterozygous effects are evident in humans but not mouse, and the homozygous effects in mouse are similar in nature to the human heterozgyous effect”
Cranial sutures as intramembranous bone growth sites (2000, background): “Conversely, mice deficient for the MSX2 gene show wide open fontanels in the cranial vault, similar to the defect seen in the human condition induced by MSX2 haploinsufficiency (Satokata et al., 2000; Wilkie et al., 2000).”
Recent advances in craniofacial morphogenesis (2006, background): “Mutation of Msx1 and Msx2 genes results in midline cleft of the first arch and severe defects in mandibular morphogenesis (Satokata et al., 2000; Ishii et al., 2005; our unpublished data).”