Cranial neural crest (CNC) cells contribute extensively to structures of the head and neck, including the palate and the calvaria (the upper part of the cranium that surrounds the brain), but the regulation of CNC cell fate during cranial development is not well understood. Members of the transforming growth factor β (TGFβ) superfamily are believed to have important regulatory roles during the development of the palate and calvaria. The TGFβ type II receptor (TGFβIIR) is expressed in CNC-derived cells during palatogenesis, as well as in the CNC-derived dura mater, the dense fibrous membrane that provides inductive signals to the developing calvaria. By using a conditional mutant, Ito et al. (see p. 5269) show that loss of Tgfbr2 expression in CNC cells results in palatal and calvaria defects caused by a lack of cell proliferation in CNC-derivatives of the palatal mesenchyme and dura mater. Intriguingly, the expression patterns of the transcription factor Msx1 and cell cycle regulator cyclin D1 are abnormal in Tgfbr2 conditional mutants, raising the possibility that TGFβ signalling interacts with these to control CNC cell proliferation.
IN THIS ISSUE|
01 November 2003
A crucial player in craniofacial development
Online Issn: 1477-9129
Print Issn: 0950-1991
© 2003.
2003
Development (2003) 130 (21): e2105.
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Conditional inactivation of Tgfbr2 in cranial neural crest causes cleft palate and calvaria defects
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A crucial player in craniofacial development. Development 1 November 2003; 130 (21): e2105. doi:
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