Transferrin receptor facilitates TGF-β and BMP signaling activation to control craniofacial morphogenesis.

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 Dis

journal_title

Cell death & disease

authors

Lei R,Zhang K,Liu K,Shao X,Ding Z,Wang F,Hong Y,Zhu M,Li H,Li H

doi

10.1038/cddis.2016.170

subject

Has Abstract

pub_date

2016-06-30 00:00:00

pages

e2282

issue

6

issn

2041-4889

pii

cddis2016170

journal_volume

7

pub_type

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