Abstract:
:The Pierre Robin Sequence (PRS), consisting of cleft palate, glossoptosis and micrognathia, is a common human birth defect. However, how this abnormality occurs remains largely unknown. Here we report that neural crest cell (NCC)-specific knockout of transferrin receptor (Tfrc), a well known transferrin transporter protein, caused micrognathia, cleft palate, severe respiratory distress and inability to suckle in mice, which highly resemble human PRS. Histological and anatomical analysis revealed that the cleft palate is due to the failure of palatal shelves elevation that resulted from a retarded extension of Meckel's cartilage. Interestingly, Tfrc deletion dramatically suppressed both transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signaling in cranial NCCs-derived mandibular tissues, suggesting that Tfrc may act as a facilitator of these two signaling pathways during craniofacial morphogenesis. Together, our study uncovers an unknown function of Tfrc in craniofacial development and provides novel insight into the etiology of PRS.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Lei R,Zhang K,Liu K,Shao X,Ding Z,Wang F,Hong Y,Zhu M,Li H,Li Hdoi
10.1038/cddis.2016.170subject
Has Abstractpub_date
2016-06-30 00:00:00pages
e2282issue
6issn
2041-4889pii
cddis2016170journal_volume
7pub_type
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