The growth and morphogenesis of the early mouse mandible: a quantitative analysis

Ramaesh, Thaya; Bard, Jonathan

doi:10.1046/j.1469-7580.2003.00210.x

Cited by 85 publications

(89 citation statements)

References 22 publications

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“…In Wnt1-Cre;Erk2 fl/fl mice the cranial base is not affected (data not shown), but mandibular morphology is severely disrupted. In wild-type mice, the mandibular primordium grows downward and lengthens from E12.5 to newborn stage (Ramaesh and Bard, 2003). This growth pattern seems to provide the tongue with physical space to move downward, and this movement closely coincides with the reorientation of the palatal shelves from a vertical to a horizontal position.…”

Section: Discussionmentioning

confidence: 99%

Disruption of the ERK/MAPK pathway in neural crest cells as a potential cause of Pierre Robin sequence

et al. 2015

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Disrupted ERK1/2 signaling is associated with several developmental syndromes in humans. To understand the function of ERK2 (MAPK1) in the postmigratory neural crest populating the craniofacial region, we studied two mouse models: Wnt1-Cre;Erk2 fl/fl and Osr2-Cre;Erk2 fl/fl . Wnt1-Cre;Erk2 fl/fl mice exhibited cleft palate, malformed tongue, micrognathia and mandibular asymmetry. Cleft palate in these mice was associated with delay/failure of palatal shelf elevation caused by tongue malposition and micrognathia. Osr2-Cre;Erk2 fl/fl mice, in which the Erk2 deletion is restricted to the palatal mesenchyme, did not display cleft palate, suggesting that palatal clefting in Wnt1-Cre; Erk2 fl/fl mice is a secondary defect. Tongues in Wnt1-Cre;Erk2 fl/fl mice exhibited microglossia, malposition, disruption of the muscle patterning and compromised tendon development. The tongue phenotype was extensively rescued after culture in isolation, indicating that it might also be a secondary defect. The primary malformations in Wnt1-Cre;Erk2 fl/fl mice, namely micrognathia and mandibular asymmetry, are linked to an early osteogenic differentiation defect. Collectively, our study demonstrates that mutation of Erk2 in neural crest derivatives phenocopies the human Pierre Robin sequence and highlights the interconnection of palate, tongue and mandible development. Because the ERK pathway serves as a crucial point of convergence for multiple signaling pathways, our study will facilitate a better understanding of the molecular regulatory mechanisms of craniofacial development.

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Section: Discussionmentioning

confidence: 99%

Disruption of the ERK/MAPK pathway in neural crest cells as a potential cause of Pierre Robin sequence

et al. 2015

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“…In the Meckel's cartilage primordium, which is also derived from neural crest cells, lacZ expression was detected only in the rostral process, a distalmost portion, at E12.5. At E12.5 to 13.5, the rostral process is rich in proliferative, undifferentiated cells, while cells start to differentiate into chondrocytes in the bilateral rod portion (Ramaesh and Bard, 2003). Thus, Ednra expression in neural-crest derivatives may be stage-and/or lineage-dependent.…”

Section: Ednra-lacz Expression In the Head Mesenchyme And Cranial Neumentioning

confidence: 99%

Recombinase-mediated cassette exchange reveals the selective use of Gq/G11-dependent and -independent endothelin 1/endothelin type A receptor signaling in pharyngeal arch development

et al. 2008

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The endothelin (Edn) system comprises three ligands (Edn1, Edn2 and Edn3) and their G-protein-coupled type A (Ednra) and type B (Ednrb) receptors. During embryogenesis, the Edn1/Ednra signaling is thought to regulate the dorsoventral axis patterning of pharyngeal arches via Dlx5/Dlx6 upregulation. To further clarify the underlying mechanism, we have established mice in which gene cassettes can be efficiently knocked-in into the Ednra locus using recombinase-mediated cassette exchange (RMCE) based on the Cre-lox system. The first homologous recombination introducing mutant lox-flanked Neo resulted in homeotic transformation of the lower jaw to an upper jaw, as expected. Subsequent RMCE-mediated knock-in of lacZ targeted its expression to the cranial/cardiac neural crest derivatives as well as in mesoderm-derived head mesenchyme. Knock-in of Ednra cDNA resulted in a complete rescue of craniofacial defects of Ednra-null mutants. By contrast, Ednrb cDNA could not rescue them except for the most distal pharyngeal structures. At early stages, the expression of Dlx5, Dlx6 and their downstream genes was downregulated and apoptotic cells distributed distally in the mandible of Ednrb-knock-in embryos. These results, together with similarity in craniofacial defects between Ednrb-knock-in mice and neural-crest-specific G␣ q /G␣ 11 -deficient mice, indicate that the dorsoventral axis patterning of pharyngeal arches is regulated by the Ednra-selective, G q /G 11 -dependent signaling, while the formation of the distal pharyngeal region is under the control of a G q /G 11 -independent signaling, which can be substituted by Ednrb. This RMCE-mediated knock-in system can serve as a useful tool for studies on gene functions in craniofacial development.

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“…This unique ossification process contrasts with the bidirectional long bone ossification process. It also demonstrates that, while the mandibular body is formed intramembranously from marrow-and periosteum-derived precursors adjacent to Meckel's cartilage (Oka et al 2007;Ramaesh and Bard 2003), most of the ramus bone can be traced to chondrocyte-derived bone cells (Figs. 2, 4d).…”

Section: Cell Lineage Tracing Demonstrates 1 Ossification Center In Tmentioning

confidence: 99%

Roles of Chondrocytes in Endochondral Bone Formation and Fracture Repair

Hinton¹,

Jing²,

Jing³

et al. 2016

J Dent Res

101

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The formation of the mandibular condylar cartilage (MCC) and its subchondral bone is an important but understudied topic in dental research. The current concept regarding endochondral bone formation postulates that most hypertrophic chondrocytes undergo programmed cell death prior to bone formation. Under this paradigm, the MCC and its underlying bone are thought to result from 2 closely linked but separate processes: chondrogenesis and osteogenesis. However, recent investigations using cell lineage tracing techniques have demonstrated that many, perhaps the majority, of bone cells are derived via direct transformation from chondrocytes. In this review, the authors will briefly discuss the history of this idea and describe recent studies that clearly demonstrate that the direct transformation of chondrocytes into bone cells is common in both long bone and mandibular condyle development and during bone fracture repair. The authors will also provide new evidence of a distinct difference in ossification orientation in the condylar ramus (1 ossification center) versus long bone ossification formation (2 ossification centers). Based on our recent findings and those of other laboratories, we propose a new model that contrasts the mode of bone formation in much of the mandibular ramus (chondrocyte-derived) with intramembranous bone formation of the mandibular body (non-chondrocyte-derived).

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The growth and morphogenesis of the early mouse mandible: a quantitative analysis

Cited by 85 publications

References 22 publications

Disruption of the ERK/MAPK pathway in neural crest cells as a potential cause of Pierre Robin sequence

Disruption of the ERK/MAPK pathway in neural crest cells as a potential cause of Pierre Robin sequence

Recombinase-mediated cassette exchange reveals the selective use of Gq/G11-dependent and -independent endothelin 1/endothelin type A receptor signaling in pharyngeal arch development

Roles of Chondrocytes in Endochondral Bone Formation and Fracture Repair

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