New directions in craniofacial morphogenesis

Szabo-Rogers, Heather L.; Smithers, Lucy; Yakob, Wardati; Liu, Karen

doi:10.1016/j.ydbio.2009.11.021

Cited by 125 publications

(121 citation statements)

References 148 publications

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“…Several rare pleiotropic diseases that affect craniofacial skeletal formation show disruption in primary cilia (20,21), and oralfacial-digital (OFD) syndrome and Bardet-Biedl syndrome (BBS) are related to ciliary dysfunction (22,23). Consistent with the findings in humans, mutations in Ofd1 in mice and zebrafish cause severe craniofacial abnormalities, including cleft palate and shortened Meckel's cartilage (22,24).…”

mentioning

confidence: 65%

“…Because epithelial-mesenchymal interactions are essential in craniofacial morphogenesis (21,27), we also deleted Ift20 in an epithelial cell-specific manner using the keratin 14 (K14)-Cre driver line (32). Epithelial-specific deletion of Ift20 (Ift20:K14-Cre) did not induce overt abnormalities in the craniofacial regions (Fig.…”

Section: Disruption Of Ift20 In Neural Crest Cells Results In Craniofmentioning

confidence: 99%

“…Growth factor signaling in CNCCs regulates the patterning and growth of facial primordia (21,27,28). Although it has been widely recognized that primary cilia are projected like antennas and serve as either chemosensory or mechanosensory organelles, their role in CNCCs remains unclear.…”

Section: Ift20 Is Essential For Assembling Primary Cilia That Transdumentioning

confidence: 99%

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Canonical and noncanonical intraflagellar transport regulates craniofacial skeletal development

Noda¹,

Kitami²,

Kitami

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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The primary cilium is a cellular organelle that coordinates signaling pathways critical for cell proliferation, differentiation, survival, and homeostasis. Intraflagellar transport (IFT) plays a pivotal role in assembling primary cilia. Disruption and/or dysfunction of IFT components can cause multiple diseases, including skeletal dysplasia. However, the mechanism by which IFT regulates skeletogenesis remains elusive. Here, we show that a neural crest-specific deletion of intraflagellar transport 20 (Ift20) in mice compromises ciliogenesis and intracellular transport of collagen, which leads to osteopenia in the facial region. Whereas platelet-derived growth factor receptor alpha (PDGFRα) was present on the surface of primary cilia in wildtype osteoblasts, disruption of Ift20 down-regulated PDGFRα production, which caused suppression of PDGF-Akt signaling, resulting in decreased osteogenic proliferation and increased cell death. Although osteogenic differentiation in cranial neural crest (CNC)-derived cells occurred normally in Ift20-mutant cells, the process of mineralization was severely attenuated due to delayed secretion of type I collagen. In control osteoblasts, procollagen was easily transported from the endoplasmic reticulum (ER) to the Golgi apparatus. By contrast, despite having similar levels of collagen type 1 alpha 1 (Col1a1) expression, Ift20 mutants did not secrete procollagen because of dysfunctional ER-to-Golgi trafficking. These data suggest that in the multipotent stem cells of CNCs, IFT20 is indispensable for regulating not only ciliogenesis but also collagen intracellular trafficking. Our study introduces a unique perspective on the canonical and noncanonical functions of IFT20 in craniofacial skeletal development.cranial neural crest cells | intracellular trafficking | intraflagellar transport | PDGF signaling | primary cilia

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mentioning

confidence: 65%

Section: Disruption Of Ift20 In Neural Crest Cells Results In Craniofmentioning

confidence: 99%

See 1 more Smart Citation

Canonical and noncanonical intraflagellar transport regulates craniofacial skeletal development

Noda¹,

Kitami²,

Kitami

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition, the expanding MxP pushes the nostrils into the more medial region. Failure or delay of outgrowth and fusion of the NPs and MxP lead to cleft lip with or without cleft palate (CL/P) (Szabo-Rogers et al, 2010;Dixon et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Wnt9b-dependent FGF signaling is crucial for outgrowth of the nasal and maxillary processes during upper jaw and lip development

et al. 2012

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SUMMARYOutgrowth and fusion of the lateral and medial nasal processes and of the maxillary process of the first branchial arch are integral to lip and primary palate development. Wnt9b mutations are associated with cleft lip and cleft palate in mice; however, the cause of these defects remains unknown. Here, we report that Wnt9b -/-mice show significantly retarded outgrowth of the nasal and maxillary processes due to reduced proliferation of mesenchymal cells, which subsequently results in a failure of physical contact between the facial processes that leads to cleft lip and cleft palate. These cellular defects in Wnt9b -/-mice are mainly caused by reduced FGF family gene expression and FGF signaling activity resulting from compromised canonical WNT/-catenin signaling. Our study has identified a previously unknown regulatory link between WNT9B and FGF signaling during lip and upper jaw development.

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“…The facial skeleton develops from the growth and fusion of multiple facial processes that are composed of neural crest and mesodermal mesenchyme surrounded by ectodermal and endodermal epithelial layers [1][2][3][4][5][6][7][8][9][10][11] . Morphogenetic events within each process are governed by distinct signaling interactions between the mesenchyme and surrounding epithelia [12][13][14][15][16] .…”

Section: Introductionmentioning

confidence: 99%

Assessing Species-specific Contributions To Craniofacial Development Using Quail-duck Chimeras

Fish

Schneider

2014

JoVE

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The generation of chimeric embryos is a widespread and powerful approach to study cell fates, tissue interactions, and species-specific contributions to the histological and morphological development of vertebrate embryos. In particular, the use of chimeric embryos has established the importance of neural crest in directing the species-specific morphology of the craniofacial complex. The method described herein utilizes two avian species, duck and quail, with remarkably different craniofacial morphology. This method greatly facilitates the investigation of molecular and cellular regulation of species-specific pattern in the craniofacial complex. Experiments in quail and duck chimeric embryos have already revealed neural crest-mediated tissue interactions and cell-autonomous behaviors that regulate species-specific pattern in the craniofacial skeleton, musculature, and integument. The great diversity of neural crest derivatives suggests significant potential for future applications of the quail-duck chimeric system to understanding vertebrate development, disease, and evolution.

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New directions in craniofacial morphogenesis

Cited by 125 publications

References 148 publications

Canonical and noncanonical intraflagellar transport regulates craniofacial skeletal development

Canonical and noncanonical intraflagellar transport regulates craniofacial skeletal development

Wnt9b-dependent FGF signaling is crucial for outgrowth of the nasal and maxillary processes during upper jaw and lip development

Assessing Species-specific Contributions To Craniofacial Development Using Quail-duck Chimeras

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