Induction of the neural crest and the opportunities of life on the edge

Huang, Xiao; Saint-Jeannet, Jean Pierre

doi:10.1016/j.ydbio.2004.07.033

Cited by 226 publications

(174 citation statements)

References 128 publications

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“…Because most of the craniofacial mesenchyme is derived from neural crest cells, genes and molecular pathways regulating neural crest formation, migration, patterning, proliferation, and apoptosis, are all important for craniofacial development. Various aspects of cranial neural crest development and the roles of neural crest in craniofacial development have been reviewed recently by others (e.g., Wilkie and Morris-Kay, 2001;Chambers and McGonnell, 2002;Basch et al, 2004;Cox, 2004;Huang and Saint-Jeannet, 2004;Graham et al, 2004;Kulesa et al, 2004;Marazita and Mooney, 2004;Helms et al, 2005). We will focus on discussing the genes and molecular pathways critical for upper lip morphogenesis after the five facial prominences have formed.…”

Section: Genes and Molecular Pathways Critical For Upper Lip Developmentmentioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

282

304

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The vertebrate upper lip forms from initially freely projecting maxillary, medial nasal, and lateral nasal prominences at the rostral and lateral boundaries of the primitive oral cavity. These facial prominences arise during early embryogenesis from ventrally migrating neural crest cells in combination with the head ectoderm and mesoderm and undergo directed growth and expansion around the nasal pits to actively fuse with each other. Initial fusion is between lateral and medial nasal processes and is followed by fusion between maxillary and medial nasal processes. Fusion between these prominences involves active epithelial filopodial and adhering interactions as well as programmed cell death. Slight defects in growth and patterning of the facial mesenchyme or epithelial fusion result in cleft lip with or without cleft palate, the most common and disfiguring craniofacial birth defect. Recent studies of craniofacial development in animal models have identified components of several major signaling pathways, including Bmp, Fgf, Shh, and Wnt signaling, that are critical for proper midfacial morphogenesis and/or lip fusion. There is also accumulating evidence that these signaling pathways cross-regulate genetically as well as crosstalk intracellularly to control cell proliferation and tissue patterning. This review will summarize the current understanding of the basic morphogenetic processes and molecular mechanisms underlying upper lip development and discuss the complex interactions of the various signaling pathways and challenges for understanding cleft lip pathogenesis.

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Section: Genes and Molecular Pathways Critical For Upper Lip Developmentmentioning

confidence: 99%

Development of the upper lip: Morphogenetic and molecular mechanisms

Jiang

Bush

Lidral

2005

Developmental Dynamics

282

304

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“…The neural crest is initially formed at the junction of the epidermal and neural ectoderm by mutual interaction between these tissues, and by signals from the mesoderm. Several molecules have been implicated in neural crest induction, including BMPs, Wnts, FGF, Notch and Retinoic Acid (for reviews, see Aybar and Mayor, 2002;Basch et al, 2004;Dorsky et al, 2000;Heeg-Truesdell and LaBonne, 2004;Huang and Saint-Jeannet, 2004;Knecht and Bronner-Fraser, 2002;Mayor and Aybar, 2001).…”

Section: Introductionmentioning

confidence: 99%

Essential role of non-canonical Wnt signalling in neural crest migration

et al. 2005

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Migration of neural crest cells is an elaborate process that requires the delamination of cells from an epithelium and cell movement into an extracellular matrix. In this work, it is shown for the first time that the non-canonical Wnt signalling [planar cell polarity (PCP) or Wnt-Ca2+] pathway controls migration of neural crest cells. By using specific Dsh mutants, we show that the canonical Wnt signalling pathway is needed for neural crest induction, while the non-canonical Wnt pathway is required for neural crest migration. Grafts of neural crest tissue expressing non-canonical Dsh mutants, as well as neural crest cultured in vitro, indicate that the PCP pathway works in a cell-autonomous manner to control neural crest migration. Expression analysis of non-canonical Wnt ligands and their putative receptors show that Wnt11 is expressed in tissue adjacent to neural crest cells expressing the Wnt receptor Frizzled7 (Fz7). Furthermore, loss- and gain-of-function experiments reveal that Wnt11 plays an essential role in neural crest migration. Inhibition of neural crest migration by blocking Wnt11 activity can be rescued by intracellular activation of the non-canonical Wnt pathway. When Wnt11 is expressed opposite its normal site of expression, neural crest migration is blocked. Finally, time-lapse analysis of cell movement and cell protrusion in neural crest cultured in vitro shows that the PCP or Wnt-Ca2+ pathway directs the formation of lamellipodia and filopodia in the neural crest cells that are required for their delamination and/or migration.

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“…Some extracellular signaling molecules such as BMP, Wnt, FGF, and Notch are believed to up-regulate specific target transcription factors that have been shown to be required for neural crest formation (LaBonne and Bronner-Fraser, 1998;Huang and Saint-Jeannet, 2004;Steventon et al, 2005;Cornell and Eisen, 2005). The combinatorial action of signaling molecules and these transcription factors defines the bona fide neural crest region (reviewed by Sauka-Spengler and Bronner-Fraser, 2006), although little is known about how these signaling molecules and transcription factors regulate neural crest induction and maintenance.…”

Section: Introductionmentioning

confidence: 99%

Xenopus hairy2 functions in neural crest formation by maintaining cells in a mitotic and undifferentiated state

Nagatomo

Hashimoto

2007

Developmental Dynamics

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The neural crest is a population of mitotically active, multipotent progenitor cells that arise at the neural plate border. Neural crest progenitors must be maintained in a multipotent state until after neural tube closure. However, the molecular underpinnings of this process have yet to be fully elucidated. Here we show that the basic helix-loop-helix (bHLH) transcriptional repressor gene, Xenopus hairy2 (Xhairy2), is an essential early regulator of neural crest formation in Xenopus. During gastrulation, Xhairy2 is localized at the presumptive neural crest prior to the expression of such neural crest markers as Slug and FoxD3. Morpholino-mediated knockdown of Xhairy2 results in the repression of neural crest marker gene expression while inducing the ectopic expression of the cell cycle inhibitor p27 xic1 in the presumptive neural crest. We also found that ectopic p27 xic1 disturbs neural crest formation. Furthermore, the depletion of Xhairy2 leads to the apoptosis of mitotic cells. Our results suggest that Xhairy2 functions in neural crest specification by maintaining cells in the mitotic and undifferentiated state.

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Induction of the neural crest and the opportunities of life on the edge

Cited by 226 publications

References 128 publications

Development of the upper lip: Morphogenetic and molecular mechanisms

Development of the upper lip: Morphogenetic and molecular mechanisms

Essential role of non-canonical Wnt signalling in neural crest migration

Xenopus hairy2 functions in neural crest formation by maintaining cells in a mitotic and undifferentiated state

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