A Stable Cranial Neural Crest Cell Line from Mouse

Ishii, Masahiko; Arias, Athena; Liu, Liqiong; Chen, Yibu; Bronner‐Fraser, Marianne; Maxson, Robert E.

doi:10.1089/scd.2012.0155

Cited by 110 publications

(135 citation statements)

References 53 publications

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“…We show in mouse cNCCs (Ishii et al, 2012) that Shh pathway activation via addition of SHH ligand or overexpression of a constitutively active form of the pathway transducer SMO causes increased Foxf2 expression, and that this induction requires GLI2. In silico screening identified a novel GLI consensus binding site 0.8 kb downstream of Foxf2, and we show that purified GLI1 protein directly binds to this site in vitro.…”

Section: Discussionmentioning

confidence: 80%

“…5A). To decipher how Shh signaling regulates Foxf2 at the cellular level, we utilized a mouse cNCC line (O9-1) that recapitulates the expression signature [AP-2α (Tfap2a), Twist1, Sox9, Cd44] and differentiation potential of the postmigrational neural crest-derived cranial mesenchyme (Ishii et al, 2012). Shh ligand (SHH) stimulation of cNCCs caused significant upregulation of both Gli1 and Foxf2 expression, which was blocked completely by the addition of vismodegib (Fig.…”

Section: Foxf2 Is a Target Of Canonical Shh Signaling In Cnccsmentioning

confidence: 99%

“…Immortalized O9-1 mouse cNCCs were cultured as described (Ishii et al, 2012). Cells were authenticated and tested for contamination.…”

Section: In Vitro Cell Culturementioning

confidence: 99%

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Sonic Hedgehog regulation of Foxf2 promotes cranial neural crest mesenchyme proliferation and is disrupted in cleft lip morphogenesis

et al. 2017

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Cleft lip is one of the most common human birth defects, yet our understanding of the mechanisms that regulate lip morphogenesis is limited. Here, we show in mice that sonic hedgehog (Shh)-induced proliferation of cranial neural crest cell (cNCC) mesenchyme is required for upper lip closure. Gene expression profiling revealed a subset of Forkhead box (Fox) genes that are regulated by Shh signaling during lip morphogenesis. During cleft pathogenesis, reduced proliferation in the medial nasal process mesenchyme paralleled the domain of reduced Foxf2 and Gli1 expression. SHH ligand induction of Foxf2 expression was dependent upon Shh pathway effectors in cNCCs, while a functional GLI-binding site was identified downstream of Foxf2. Consistent with the cellular mechanism demonstrated for cleft lip pathogenesis, we found that either SHH ligand addition or FOXF2 overexpression is sufficient to induce cNCC proliferation. Finally, analysis of a large multi-ethnic human population with cleft lip identified clusters of single-nucleotide polymorphisms in FOXF2. These data suggest that direct targeting of Foxf2 by Shh signaling drives cNCC mesenchyme proliferation during upper lip morphogenesis, and that disruption of this sequence results in cleft lip.

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Section: Discussionmentioning

confidence: 80%

Section: Foxf2 Is a Target Of Canonical Shh Signaling In Cnccsmentioning

confidence: 99%

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Sonic Hedgehog regulation of Foxf2 promotes cranial neural crest mesenchyme proliferation and is disrupted in cleft lip morphogenesis

et al. 2017

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“…Cre ; R26R-green fluorescent protein (GFP)-expressing cells and can differentiate into multiple CNC derivatives, including osteoblasts, chondrocytes, smooth muscle cells and glial cells (Ishii et al, 2012). To examine cell proliferation in response to altered Hippo signaling, we used siRNA-mediated knockdown to reduce expression of Yap and Taz, as well as Lats1 and Lats2, in O9-1 cells, and performed pHH3 immunofluorescence staining to assess cell proliferation.…”

Section: Wnt1mentioning

confidence: 99%

“…Importantly, the medium was conditioned with growth-inhibited STO (mouse embryonic fibroblast cell line) feeder cells overnight, filtered (0.22 µm pore size) and further supplemented with 25 ng/ml basic fibroblast growth factor (R&D Systems, 233-FB) and 1000 U leukemia inhibitory factor (Millipore, ESG1106). The conditions used for smooth muscle differentiation were described previously (Ishii et al, 2012). For the siRNA knockdown experiments in O9-1 cells, siRNA SMARTpools targeting Yap, Taz and Hippo kinases Lats1 and Lats2 were purchased from Dharmacon and the transfections were performed by following a typical RNAiMAX transfection procedure (Thermo Fisher Scientific).…”

Section: O9-1 Cell Culture and Sirna Knockdownmentioning

confidence: 99%

Yap and Taz play a crucial role in neural crest-derived craniofacial development

et al. 2015

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The role of the Hippo signaling pathway in cranial neural crest (CNC) development is poorly understood. We used the Wnt1Cre and Wnt1Cre2SOR drivers to conditionally ablate both Yap and Taz in the CNC of mice. When using either Cre driver, Yap and Taz deficiency in the CNC resulted in enlarged, hemorrhaging branchial arch blood vessels and hydrocephalus. However, Wnt1Cre2SOR embryos had an open cranial neural tube phenotype that was not evident in Wnt1Cre embryos. In O9-1 CNC cells, the loss of Yap and Taz impaired smooth muscle cell differentiation. RNA-sequencing data indicated that Yap and Taz regulate genes encoding Fox transcription factors, specifically Foxc1. Proliferation was reduced in the branchial arch mesenchyme of Yap and Taz CNC conditional knockout (CKO) embryos. Moreover, Yap and Taz CKO embryos had cerebellar aplasia similar to Dandy Walker spectrum malformations observed in human patients and mouse embryos with mutations in Foxc1. In embryos and O9-1 cells deficient for Yap and Taz, Foxc1 expression was significantly reduced. Analysis of Foxc1 regulatory regions revealed a conserved recognition element for the Yap and Taz DNA binding co-factor Tead. ChIP-pcr experiments further supported the conclusion that Foxc1 is directly regulated by the Yap/Tead complex. Our findings uncover important roles for Yap and Taz in CNC diversification and development.

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Cranial neural crest cell contribution to craniofacial formation, pathology, and future directions in tissue engineering

Snider

Mishina

2014

Birth Defects Research Pt C

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This review provides an overview of the state and future directions of development and pathology in the craniofacial complex in the context of Cranial Neural Crest Cells (CNCC). CNCC are a multipotent cell population that is largely responsible for forming the vertebrate head. We focus on findings that have increased the knowledge of gene regulatory networks and molecular mechanisms governing CNCC migration and the participation of these cells in tissue formation. Pathology due to aberrant migration or cell death of CNCC, termed neurocristopathies, is discussed in addition to craniosynostoses. Finally, we discuss tissue engineering applications that take advantage of recent advancements in genome editing and the multipotent nature of CNCC. These applications have relevance to treating diseases due directly to the failure of CNCC, and also in restoring tissues lost due to a variety of reasons.

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A Stable Cranial Neural Crest Cell Line from Mouse

Cited by 110 publications

References 53 publications

Sonic Hedgehog regulation of Foxf2 promotes cranial neural crest mesenchyme proliferation and is disrupted in cleft lip morphogenesis

Sonic Hedgehog regulation of Foxf2 promotes cranial neural crest mesenchyme proliferation and is disrupted in cleft lip morphogenesis

Yap and Taz play a crucial role in neural crest-derived craniofacial development

Cranial neural crest cell contribution to craniofacial formation, pathology, and future directions in tissue engineering

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