Mandible and Tongue Development

Parada, Carolina; Chai, Yang

doi:10.1016/bs.ctdb.2015.07.023

Cited by 136 publications

(162 citation statements)

References 106 publications

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“…The MC provides a scaffold for the differentiating mandibular osteoblasts and serves also as a driving force for the outgrowth of the jaw. Mesenchymal cells surrounding the MC differentiate into osteoblasts and deposit bone matrix for the future mandible (Parada and Chai, 2015, Ramaesh and Bard, 2003). VEGF from CNC cells and their derivatives supports MC extension, enhances vascularization of the jaw, and stabilizes major mandibular arteries.…”

Section: Vegf In Skeletal Developmentmentioning

confidence: 99%

Vascular endothelial growth factor control mechanisms in skeletal growth and repair

Olsen

2016

Developmental Dynamics

102

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Vascular Endothelial Growth factor A (VEGF) is a critical regulator of vascular development, postnatal angiogenesis and homeostasis, and it is essential for bone development and repair. Blood vessels serve both as structural templates for bone formation and they provide essential cells, growth factors and minerals needed for synthesis and mineralization, as well as turnover, of the extracellular matrix in bone. Through its regulation of angiogenesis, VEGF contributes to coupling of osteogenesis to angiogenesis, and it directly controls the differentiation and function of osteoblasts and osteoclasts. In this review we summarize the properties of VEGF and its receptors that are relevant to bone formation and repair; the roles of VEGF during development of endochondral and membranous bones; and the contributions of VEGF to bone healing during different phases of bone repair. Finally, we discuss contributions of altered VEGF function in inherited disorders with bone defects as part of their phenotypes, and we speculate on what will be required before therapeutic strategies based on VEGF modulation can be developed for clinical use to treat patients with bone growth disorders and/or compromised bone repair.

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Section: Vegf In Skeletal Developmentmentioning

confidence: 99%

Vascular endothelial growth factor control mechanisms in skeletal growth and repair

Olsen

2016

Developmental Dynamics

102

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“…Development of the tongue begins with the emergence of a swelling composed of NCCs on the floor mandible called the median lingual swelling (Parada et al, 2012; Salles et al, 2008). During this stage, the vast majority of the tongue anlage is composed of NCC-derived mesenchymal cells (Han et al, 2012; Parada and Chai, 2015; Parada et al, 2012). Subsequently, bilateral elevations called the lateral lingual swellings emerge on either side of the medial lingual swelling.…”

Section: Introductionmentioning

confidence: 99%

“…Non-canonical and canonical Transforming Growth Factor-β (TGF-β) signaling in NCCs have been reported to control the proliferation and organization of glossal muscles, after the formation of the tongue bud (Hosokawa et al, 2010; Parada and Chai, 2015). Hand2, via the negative regulation of Dlx5 and Dlx6 expression in the distal arch ectomesenchyme, patterns the distal portion of the mandible and is essential in the initiation of the tongue mesenchyme morphogenesis (Barron et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Cilia-dependent GLI processing in neural crest cells is required for tongue development

Millington¹,

Elliott²,

Chang³

et al. 2017

Developmental Biology

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Ciliopathies are a class of diseases caused by the loss of a ubiquitous, microtubule-based organelle called a primary cilium. Ciliopathies commonly result in defective development of the craniofacial complex, causing midfacial defects, craniosynostosis, micrognathia and aglossia. Herein, we explored how the conditional loss of primary cilia on neural crest cells (Kif3af/f;Wnt1-Cre) generated aglossia. On a cellular level, our data revealed that aglossia in Kif3af/f;Wnt1-Cre embryos was due to a loss of mesoderm-derived muscle precursors migrating into and surviving in the tongue anlage. To determine the molecular basis for this phenotype, we performed RNA-seq, in situ hybridization, qPCR and Western blot analyses. We found that transduction of the Sonic hedgehog (Shh) pathway, rather than other pathways previously implicated in tongue development, was aberrant in Kif3af/f;Wnt1-Cre embryos. Despite increased production of full-length GLI2 and GLI3 isoforms, previously identified GLI targets important for mandibular and glossal development (Foxf1, Foxf2, Foxd1 and Foxd2) were transcriptionally downregulated in Kif3af/f;Wnt1-Cre embryos. Genetic removal of GLI activator (GLIA) isoforms in neural crest cells recapitulated the aglossia phenotype and downregulated Fox gene expression. Genetic addition of GLIA isoforms in neural crest cells partially rescued the aglossia phenotype and Fox gene expression in Kif3af/f;Wnt1-Cre embryos. Together, our data suggested that glossal development requires primary cilia-dependent GLIA activity in neural crest cells. Furthermore, these data, in conjunction with our previous work, suggested prominence specific roles for GLI isoforms; with development of the frontonasal prominence relying heavily on the repressor isoform and the development of the mandibular prominence/tongue relying heavily on the activator isoform.

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“…Morphogenetic events in murine palatogenesis, particular in the elevation of the palatal shelves from a vertical to a horizontal position, depends on both intrinsic factors from the shelf itself and the extrinsic forces coinciding with the downward movement of the tongue (2,13,41). Proper cell proliferation is essential for the proper growth of craniofacial structures.…”

Section: Discussionmentioning

confidence: 99%

“…Clinically, it is referred to as the Pierre Robin sequence (PRS), which is comprised of mandibular hypoplasia (micrognathia or retrognathia), displaced tongue position, and cleft secondary palate (5). Previous studies from a few mutant mouse strains, including deficiencies in Hoxa2, Snail1/2, Prdm16, Alk2, Sox9, and Erk2, have shown that the cleft secondary palate resulting from the failed palatal elevation is a consequence of the physical obstruction by a malpositioned tongue (6 -12), partially mimicking the clefting of PRS in humans (2,13,14). In many of the murine mutant models of PRS-like clefting, the expression of the gene of interest is detected in the palatal shelves themselves in addition to the relevant structure, like the mandible (2).…”

mentioning

confidence: 99%

Ablation of the Sox11 Gene Results in Clefting of the Secondary Palate Resembling the Pierre Robin Sequence

Huang

Xiao

Bao

et al. 2016

Journal of Biological Chemistry

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Mouse gene inactivation has shown that the transcription factor Sox11 is required for mouse palatogenesis. However, whether Sox11 is primarily involved in the regulation of palatogenesis still remains elusive. In this study, we explored the role of Sox11 in palatogenesis by analyzing the developmental mechanism in cleft palate formation in mutants deficient in Sox11. Sox11 is expressed both in the developing palatal shelf and in the surrounding structures, including the mandible. We found that cleft palate occurs only in the mutant in which Sox11 is directly deleted. As in the wild type, the palatal shelves in the Sox11 mutant undergo outgrowth in a downward direction and exhibit potential for fusion and elevation. However, mutant palatal shelves encounter clefting, which is associated with a malpositioned tongue that results in physical obstruction of palatal shelf elevation at embryonic day 14.5 (E14.5). We found that loss of Sox11 led to reduced cell proliferation in the developing mandibular mesenchyme via Cyclin D1, leading to mandibular hypoplasia, which blocks tongue descent. Extensive analyses of gene expression in Sox11 deficiency identified FGF9 as a potential candidate target of Sox11 in the modulation of cell proliferation both in the mandible and the palatal shelf between E12.5 and E13.5. Finally we show, using in vitro assays, that Sox11 directly regulates the expression of Fgf9 and that application of FGF9 protein to Sox11-deficient palatal shelves restores the rate of BrdU incorporation. Taken together, the palate defects presented in the Sox11 loss mutant mimic the clefting in the Pierre Robin sequence in humans.

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Mandible and Tongue Development

Cited by 136 publications

References 106 publications

Vascular endothelial growth factor control mechanisms in skeletal growth and repair

Vascular endothelial growth factor control mechanisms in skeletal growth and repair

Cilia-dependent GLI processing in neural crest cells is required for tongue development

Ablation of the Sox11 Gene Results in Clefting of the Secondary Palate Resembling the Pierre Robin Sequence

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