Готові списки джерел за темами / Craniofacial morphogenesis

Добірка наукової літератури з теми "Craniofacial morphogenesis"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 28 січня 2023

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Статті в журналах з теми "Craniofacial morphogenesis"

1

Klueber, Kathleen M. "Craniofacial Morphogenesis." Ear, Nose & Throat Journal 71, no. 10 (October 1992): 472–76. http://dx.doi.org/10.1177/014556139207101008.

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2

Cobourne, M. "Review: Craniofacial Morphogenesis." European Journal of Orthodontics 25, no. 2 (April 1, 2003): 214–15. http://dx.doi.org/10.1093/ejo/25.2.214.

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3

Solursh, Michael, and Jeffrey Murray. "Craniofacial Morphogenesis Workshop Report." Cleft Palate-Craniofacial Journal 31, no. 3 (May 1994): 230–31. http://dx.doi.org/10.1597/1545-1569(1994)031<0230:cmwr>2.3.co;2.

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4

Solursh, Michael, and Jeffrey Murray. "Craniofacial Morphogenesis Workshop Report." Cleft Palate-Craniofacial Journal 31, no. 3 (May 1994): 230–31. http://dx.doi.org/10.1597/1545-1569_1994_031_0230_cmwr_2.3.co_2.

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The following report highlights the discussions and Interaction at the workshop on craniofacial morphogenesis, sponsored by The Human Frontier Science Program, held in April 1993 at the University of Iowa. A brief summary of selected sessions is Included to exemplify the benefits of bringing together Individuals from various disciplines and backgrounds In order to establish a unified theory of craniofacial morphogenesis. The synthesis of information and experience of a wide range of approaches made the 4-day period an Invaluable experience for the participants from nine different countries.
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5

Radlanski, RJ. "Prenatal craniofacial morphogenesis: four-dimensional visualization of morphogenetic processes." Orthodontics & Craniofacial Research 6 (August 2003): 89–94. http://dx.doi.org/10.1034/j.1600-0544.2003.240.x.

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6

Mundhada, A., U. Kulkarni, V. Swami, S. Deshmukh, and A. Patil. "Craniofacial Muscles-differentiation and Morphogenesis." Annual Research & Review in Biology 9, no. 6 (January 10, 2016): 1–9. http://dx.doi.org/10.9734/arrb/2016/24329.

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7

Helms, J. A. "New insights into craniofacial morphogenesis." Development 132, no. 5 (February 2, 2005): 851–61. http://dx.doi.org/10.1242/dev.01705.

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8

Szabo-Rogers, Heather L., Lucy E. Smithers, Wardati Yakob, and Karen J. Liu. "New directions in craniofacial morphogenesis." Developmental Biology 341, no. 1 (May 2010): 84–94. http://dx.doi.org/10.1016/j.ydbio.2009.11.021.

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9

Chai, Yang, and Robert E. Maxson. "Recent advances in craniofacial morphogenesis." Developmental Dynamics 235, no. 9 (2006): 2353–75. http://dx.doi.org/10.1002/dvdy.20833.

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10

Lu, Chung-Ling, and Jinoh Kim. "Craniofacial Diseases Caused by Defects in Intracellular Trafficking." Genes 12, no. 5 (May 13, 2021): 726. http://dx.doi.org/10.3390/genes12050726.

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Cells use membrane-bound carriers to transport cargo molecules like membrane proteins and soluble proteins, to their destinations. Many signaling receptors and ligands are synthesized in the endoplasmic reticulum and are transported to their destinations through intracellular trafficking pathways. Some of the signaling molecules play a critical role in craniofacial morphogenesis. Not surprisingly, variants in the genes encoding intracellular trafficking machinery can cause craniofacial diseases. Despite the fundamental importance of the trafficking pathways in craniofacial morphogenesis, relatively less emphasis is placed on this topic, thus far. Here, we describe craniofacial diseases caused by lesions in the intracellular trafficking machinery and possible treatment strategies for such diseases.
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Більше джерел

Дисертації з теми "Craniofacial morphogenesis"

1

Coussens, Anna Kathleen. "Molecular regulation of calvarial suture morphogenesis and human craniofacial diversity." Thesis, Queensland University of Technology, 2007. https://eprints.qut.edu.au/16481/1/Anna_Coussens_Thesis.pdf.

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This body of work is concerned with the genetics of craniofacial morphology and specifically with that of the cranial sutures which form fibrous articulations between the calvarial bones. The premature fusion of these sutures, known as craniosynostosis, is a common developmental abnormality and has been extensively utilised here as a tool through which to study the genetics of suture morphogenesis and craniofacial diversity. Investigations began with a search for polymorphisms associated with normal variation in human craniofacial characteristics. Denaturing High-Performance Liquid chromatography was used to identify polymorphisms in two genes causative for craniosynostosis by analysing DNA from a large cohort of individuals from four ethnogeographic populations. A single nucleotide polymorphism in fibroblast growth factor receptor 1 was identified as being associated with variation in the cephalic index, a common measure of cranial shape. To further, and specifically, investigate the molecular processes of suture morphogenesis gene expression was compared between unfused and prematurely fusing/fused suture tissues isolated from patients with craniosynostosis. Two approaches, both utilising Affymetrix gene expression microarrays, were used to identify genes differentially expressed during premature suture fusion. The first was a novel method which utilised the observation that explant cells from both fused and unfused suture tissue, cultured in minimal medium, produce a gene expression profile characteristic of minimally differentiated osteoblastic cells. Consequently, gene expression was compared between prematurely fused suture tissues and their corresponding in vitro de-differentiated cells. In addition to those genes known to be involved in suture morphogenesis, a large number of novel genes were identified which were up-regulated in the differentiated in vivo state and are thus implicated in premature suture fusion and in vivo osteoblast differentiation. The second microarray study involved an extensive analysis of 16 suture tissues and compared gene expression between unfused (n=9) and fusing/fused sutures (n=7). Again, both known genes and a substantially large number of novel genes were identified as being differentially expressed. Some of these novel genes included retinol binding protein 4 (RBP4), glypican 3 (GPC3), C1q tumour necrosis factor 3 (C1QTNF3), and WNT inhibitory factor 1 (WIF1). The known functions of these genes are suggestive of potential roles in suture morphogenesis. Realtime quantitative RT PCR (QRT-PCR) was used to verify the differential expression patterns observed for 11 genes and Western blot analysis and confocal microscopy was used to investigate the protein expression for 3 genes of interest. RBP4 was found to be localised on the ectocranial surface of unfused sutures and in cells lining the osteogenic fronts while GPC3 was localised to suture mesenchyme of unfused sutures. A comparison between each unfused suture (coronal, sagittal, metopic, and lambdoid) demonstrated that gene expression profiles are suture-specific which, based on the identification of differentially expressed genes, suggests possible molecular bases for the differential timing of normal fusion and the response of each suture to different craniosynostosis mutations. One observation of particular interest was the presence of cartilage in unfused lambdoid sutures, suggesting a role for chondrogenesis in posterior skull sutures which have generally been thought to develop by intramembranous ossification without a cartilage precursor. Finally, the effects of common media supplements used in in vitro experiments to stimulate differentiation of calvarial suture-derived cells were investigated with respect to their ability to induce in vivo-like gene expression. The response to standard differentiation medium (ascorbic acid + β-glycerophosphate) with and without dexamethasone was measured by both mineralisation and matrix formation assays and QRT-PCR of genes identified in the above described microarray studies. Both media induced collagen matrix and bone nodule formation indicative of differentiating osteoblasts. However, the genes expression profiles induced by both media differed and neither recapitulated the levels and profiles of gene expression observed in vivo for cells isolated from both fused and unfused suture tissues. This study has implications for translating results from in vitro work to the in vivo situation. Significantly, the dedifferentiation microarray study identified differentially expressed genes whose products may be considered candidates as more appropriate osteogenic supplements that may be used during in vitro experiments to better induce in vivo-like osteoblast differentiation. This study has made a substantial contribution to the identification of novel genes and pathways involved in controlling human suture morphogenesis and craniofacial diversity. The results from this research will stimulate new areas of inquiry which will one day aid in the development of better diagnostics and therapeutics for craniosynostosis, and other craniofacial and more general skeletal abnormalities.
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2

Coussens, Anna Kathleen. "Molecular regulation of calvarial suture morphogenesis and human craniofacial diversity." Queensland University of Technology, 2007. http://eprints.qut.edu.au/16481/.

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Анотація:
This body of work is concerned with the genetics of craniofacial morphology and specifically with that of the cranial sutures which form fibrous articulations between the calvarial bones. The premature fusion of these sutures, known as craniosynostosis, is a common developmental abnormality and has been extensively utilised here as a tool through which to study the genetics of suture morphogenesis and craniofacial diversity. Investigations began with a search for polymorphisms associated with normal variation in human craniofacial characteristics. Denaturing High-Performance Liquid chromatography was used to identify polymorphisms in two genes causative for craniosynostosis by analysing DNA from a large cohort of individuals from four ethnogeographic populations. A single nucleotide polymorphism in fibroblast growth factor receptor 1 was identified as being associated with variation in the cephalic index, a common measure of cranial shape. To further, and specifically, investigate the molecular processes of suture morphogenesis gene expression was compared between unfused and prematurely fusing/fused suture tissues isolated from patients with craniosynostosis. Two approaches, both utilising Affymetrix gene expression microarrays, were used to identify genes differentially expressed during premature suture fusion. The first was a novel method which utilised the observation that explant cells from both fused and unfused suture tissue, cultured in minimal medium, produce a gene expression profile characteristic of minimally differentiated osteoblastic cells. Consequently, gene expression was compared between prematurely fused suture tissues and their corresponding in vitro de-differentiated cells. In addition to those genes known to be involved in suture morphogenesis, a large number of novel genes were identified which were up-regulated in the differentiated in vivo state and are thus implicated in premature suture fusion and in vivo osteoblast differentiation. The second microarray study involved an extensive analysis of 16 suture tissues and compared gene expression between unfused (n=9) and fusing/fused sutures (n=7). Again, both known genes and a substantially large number of novel genes were identified as being differentially expressed. Some of these novel genes included retinol binding protein 4 (RBP4), glypican 3 (GPC3), C1q tumour necrosis factor 3 (C1QTNF3), and WNT inhibitory factor 1 (WIF1). The known functions of these genes are suggestive of potential roles in suture morphogenesis. Realtime quantitative RT PCR (QRT-PCR) was used to verify the differential expression patterns observed for 11 genes and Western blot analysis and confocal microscopy was used to investigate the protein expression for 3 genes of interest. RBP4 was found to be localised on the ectocranial surface of unfused sutures and in cells lining the osteogenic fronts while GPC3 was localised to suture mesenchyme of unfused sutures. A comparison between each unfused suture (coronal, sagittal, metopic, and lambdoid) demonstrated that gene expression profiles are suture-specific which, based on the identification of differentially expressed genes, suggests possible molecular bases for the differential timing of normal fusion and the response of each suture to different craniosynostosis mutations. One observation of particular interest was the presence of cartilage in unfused lambdoid sutures, suggesting a role for chondrogenesis in posterior skull sutures which have generally been thought to develop by intramembranous ossification without a cartilage precursor. Finally, the effects of common media supplements used in in vitro experiments to stimulate differentiation of calvarial suture-derived cells were investigated with respect to their ability to induce in vivo-like gene expression. The response to standard differentiation medium (ascorbic acid + β-glycerophosphate) with and without dexamethasone was measured by both mineralisation and matrix formation assays and QRT-PCR of genes identified in the above described microarray studies. Both media induced collagen matrix and bone nodule formation indicative of differentiating osteoblasts. However, the genes expression profiles induced by both media differed and neither recapitulated the levels and profiles of gene expression observed in vivo for cells isolated from both fused and unfused suture tissues. This study has implications for translating results from in vitro work to the in vivo situation. Significantly, the dedifferentiation microarray study identified differentially expressed genes whose products may be considered candidates as more appropriate osteogenic supplements that may be used during in vitro experiments to better induce in vivo-like osteoblast differentiation. This study has made a substantial contribution to the identification of novel genes and pathways involved in controlling human suture morphogenesis and craniofacial diversity. The results from this research will stimulate new areas of inquiry which will one day aid in the development of better diagnostics and therapeutics for craniosynostosis, and other craniofacial and more general skeletal abnormalities.
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3

Li, Wai-Yee. "TGF-B Signalling in Epithelial-Mesenchymal Interactions : Craniofacial Morphogenesis and Fetal Wound Healing." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.503632.

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4

Sun, Zhao. "New molecular mechanisms controlling dental epithelial stem cell maintenance, growth and craniofacial morphogenesis." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/5652.

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The regenerative tissues such as hair follicles, intestine and teeth have a particular microenvironment known as “stem cell niche” which houses stem cells and act as a signaling center to control stem cell fate. The precise and timely regulation of stem cell renewal and differentiation is essential for tissue formation, growth and homeostasis over the course of a lifetime. However, the molecular underpinning to control this regulation is poorly understood. To address this issue, we use the continuously growing mouse incisor as a model to study the gene regulatory network which controls dental epithelial stem cell (DESC) maintenance, growth and craniofacial morphogenesis. We found FoxO6, a transcription factor mainly expressed in the brain and craniofacial region, control DESC proliferation by regulating Hippo signaling. FoxO6 loss-of-function mice undergo increases in cell proliferation which finally leads to lengthening of the incisors, expansion of the face and skull and enlargement of the mandible and maxilla. We have screened three human FOXO6 single nucleotide polymorphisms which are associated with facial morphology ranging from retrognathism to prognathism. Our study also reveals that Sox2 and Lef-1, two markers for early craniofacial development, are regulated by Pitx2 to control DESC maintenance, differentiation and craniofacial development. Conditional Sox2 deletion in the oral and dental epithelia results in severe craniofacial defects, including ankyloglossia, cleft palate, arrested incisor development and abnormal molar development. The loss of Sox2 in DESCs leads to impaired stem cell proliferation, migration and subsequent dissolution of the tooth germ. On the other hand, conditional overexpression of Lef-1 in oral and dental epithelial region increases DESC proliferation and creates a new labial cervical loop stem cell compartment in dental epithelial stem cell niche, which produces rapidly growing long “tusk-like” incisors. Interestingly, Lef-1 overexpression rescues the tooth arrest defects but not the ankyloglossia or cleft palate in Sox2 conditional deletion mice. Our data also reveal that miRNA and histone remodeler are involved in regulating DESC proliferation and craniofacial morphogenesis. We describe a miR-23a/b:Hmgn2:Pitx2 signaling pathway in regulating dental epithelial cell growth and differentiation. Pitx2 activates expression of amelogenin which is the major protein component for enamel deposition. This activation can be repressed by the chromatin-associated factor Hmgn2. miR-23a and miR-23b directly target Hmgn2, leading to the release of the Hmgn2 inhibition of Pitx2 transcriptional activity and thus enhance Amelogenin production. Phenotypically, ablation of Hmgn2 in mice results in an overgrowth of incisors with increased Amelogenin expression. The findings in this study increase our current understanding of the molecular regulation of dental epithelial stem cell fate. It not only highlights new gene regulatory network that controls dental stem cell maintenance, growth and craniofacial morphogenesis, but also sheds new light on developing novel stem cell therapy or gene therapy for tooth regeneration and dental diseases.
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5

Katsube, Motoki. "Critical Growth Processes for the Midfacial Morphogenesis in the Early Prenatal Period." Kyoto University, 2019. http://hdl.handle.net/2433/242383.

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6

Alrajeh, Moussab. "Embryologie de la neurofibromatose de type I : morphogenese craniofaciale et regulations du gene NF1 dans la crete neurale." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS471/document.

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La neurofibromatose type1 (maladie de Von-Rechlinghausen) est une affection autosomique dominante, causée par des mutations polymorphes du gène NF1, dont la protéine, la Neurofibromine, agit comme un suppresseur de tumeur en opérant une contrôle négatif des protéines de RAS. D’un point de vue embryologique, cette maladie affecte les dérivés de la crête neurale (CN), une structure embryonnaire pluripotente, capable de générer des dérivés variés tels que des neurones, des cellules gliales, périvascullaires, squelettiques et pigmentaires. Les cellules de la CN subsistent aussi chez l’adulte, à l’état de cellule souches, pouvant être impliqués dans des processus régénératifs. Toutefois, lorsque leur programme morphogénétique est altéré, elles peuvent générer des processus tumoraux, à l’origine de tumeurs multiples dans la peau, les nerfs (tumeurs bénignes et malignes des gaines nerveuses, neurofibromes,) et le cerveau (50% des cas de tumeurs cérébrales avec un tiers de gliomes des voies optique sont cancéreuses). La compréhension des mécanismes de cette maladie est limitée par la faible corrélation qui existe entre génotypes et phénotypes, à savoir l’adéquation entre la nature hautement polymorphe des anomalies génétiques et la diversité des manifestations cliniques. L’objectif de l’étude est d’analyser les conséquences de l’invalidation du gène NF1 sur le comportement des cellules de la CN (CCN), leur prolifération, leur capacité de migration et leur potentiel de différenciation, chez un modèle expérimental. De plus, nous tentons d’élucider l’impact des modulations épigénétiques de l‘activité du NF1.Nous avons développé un système qui permet l’inactivation totale du gène NF1 dans les cellules de la CN spécifiquement en utilisant des molécules d’ARN interférent (silencing) transfectées par éléctroporation bilatérale dans les CCN, au stade précoce de la neurulation, en utilisant l’embryon de poulet comme modèle expérimental. Suite à l’invalidation du gène NF1, nous avons obtenus des déficits multi-systémiques qui consistent principalement en des altérations de la gangliogénèse céphalique, avec des phénotypes gliomateux, mais aussi des défauts périvasculaires qui affectent tant les parois adventitielles des artères branchiales, que les péricytes des capillaire faciaux et cérébraux, associés des asymétries faciales et des formations néoplasiques intra-cérébrales. Précocement, nous montrons que ces déficits peuvent être corrélés aux altérations du comportement migratoire, prolifératif et apoptotiques des cellules de la CN.Parallèlement, nous avons cherché à déterminer l’implication des régulations épigénétiques sur l’activité de NF1. Nous nous sommes focalisé sur l’activité des Histones Désacétylases (HDAC), qui contrôlent la configuration chromatinienne. Il s’avère que les transcrits de la classe I de famille des HDACs, les HDAC1, 2 et 8, normalement accumulés dans les CCN au cours de leur migration et selon un patron d’expression spatial et temporal similaire à celui de NF1, présentent des variations significatives suite au silencing de NF1. Nous avons testé l’inactivation sélective de ces gènes; Ainsi, nous montrons que l’invalidation de HDAC8 seule, permet de reproduire les altérations des phénotypes vasculaires observés chez les embryons hypomorphes pour NF1. Qui suggère un rôle prépondérant de HDAC8 dans la régulation de la vasculogenèse et de la différentiation des CCN en péricytes. Qui pourrait être par l’activation ectopique des gènes Sox9 soutenant la transdifférenciaton pathologique des péricytes en processus gliomateux ou en calcifications intracérébrales
The neurofibromatosis-type 1 (NF1) (Von Recklinghausen disease) is an autosomal disorder, which stems from misrgulation of Neurofibromin (NF1), a gene encoding a tumour-suppressor protein which acts as a negative regulator of RAS proteins. Mutations of NF1 are causally linked to many types of tumours located in skin, nerves, but also in the brain (intra- cerebral tumours and gliomas). NF1 patients have a high risk of developing both benign and malignant tumours. The diversity of deficits and the nature of cellular lineages attribute all these tumoral manifestations to deregulation of neural crest cell (NC) derivatives. The NC is a multipotent stem cell population that contributes to a variety of cell types in vertebrate embryo, which include skeletogenic, glial, pigment cells as well as pericytes. In order to understand the pathologic process of this disease, it is essential to analyze the molecular mechanisms involved in the survival, proliferation and differentiation of NC.Our objectives are therefore to gain insights into the molecular cascade responsible for the diversity of NC derivatives at cephalic level. We opt for a drastic approach consisting in eradicating NF1 activity from NC at the beginning of their migration. In our experimental model, we can analyze developmental interactions of NC and the epigenetic regulation of the NF1 gene, at their level. Espically class1 Histone deacetylases (HDAC) family of molecules. So we have developed a system which allows complete inactivation of the NF1 gene in NC specifically using interfering RNA molecules (silencing) transfected by electroporation in the bilateral NC, during the early stage of neurulation, using the chick embryo as an experimental model.We show that HDAC8 inactivation can reproduce the alterations of vascular phenotypes observed in NF1 hypomorphic embryos. Suggesting an important role of HDAC8 in regulating vasculogenesis and differentiation of pericytes NC. That could be by ectopic activation of Sox9 gene supporting the pathological transdifférenciaton pericytes in gliomateux process or intracerebral calcifications
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7

"Epithelial signals regulate pigpen expression during craniofacial morphogenesis." Tulane University, 2002.

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Peptide growth factors mediate epithelial-mesenchytnal interactions during organogenesis. In vitro, the expression of Pigpen, a nuclear protein, was shown to correlate with growth factor-mediated changes in proliferation and differentiation in bovine endothelial cells (Alliegro and Alliegro, 1996b). Although a number of functions have been proposed for Pigpen, the role Pigpen might play during growth factor-mediated inductive events during embryogenesis has not been determined. To begin to elucidate the role of pigpen in mouse embryogenesis. I cloned the mouse homologue of pigpen and investigated the regulation of its expression during embryogenesis. Sequence analysis of the mouse cDNA indicated that it was 89% and 95% identical to the bovine homologue at the nucleotide and amino acid levels, respectively. Immunocytochemical studies demonstrated that pigpen expression was concentrated in large nuclear granules in mouse embryonic cells, and CAT assays showed that the putative transcriptional activation domain in the 5 ' end of the protein was active in vitro. In situ hybridization analyses demonstrated that pigpen showed a ubiquitous expression pattern early in postimplantation development [on embryonic day 9.5 (E9.5)], which was followed by a pattern of more restricted expression during later organogenesis. At E10.5 pigpen expression was elevated in the mandible, other facial primordia, the limbs, and in the neural epithelium, and by E13.5 pigpen was strongly expressed in the retina, trigeminal ganglion, and dorsal root ganglion. The pattern of pigpen expression was striking in a number of organ primordia including the tooth, vibrissae, eye, lung, and kidney. Because growth factor-mediated epithelial-mesenchymal interactions are vital for the formation of all these organs, I asked how such interactions might regulate pigpen expression at a specific site, that is, in the developing mandible. In vitro assays indicated that epithelial signals were required to maintain pigpen expression in the mandibular mesenchyme and bead implantation assays demonstrated that FGF-8, and to a lesser extent FGF-9, positively regulated pigpen expression in the mesenchyme. In contrast, BMP-4 repressed the expression of pigpen. These data suggest that mouse pigpen operates downstream of specific growth factors and could activate genetic pathways that regulate proliferation and/or differentiation during craniofacial morphogenesis in the mouse embryo
acase@tulane.edu
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8

Billmyre, Katherine Kretovich. "Multiple roles of epithelial signaling during craniofacial and foregut morphogenesis." Diss., 2015. http://hdl.handle.net/10161/9827.

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Abstract

During embryonic development many structures crucial for breathing and eating arise from the pharyngeal and anterior foregut epithelium (FGE), which contains the oral ectoderm and the foregut endoderm. Proper differentiation and signaling within and from this epithelial tissue is necessary for the development of the mandible, the esophagus, and the trachea. Many birth defects occur in these structures that greatly disrupt the ability of affected infants to breathe and eat. This dissertation investigates the importance of the pharyngeal and anterior FGE in mandible and foregut development.

The most rostral portion of the pharyngeal epithelium contributes to the development of the mandible. At embryonic day 10.5 the mandible is a bud structure, composed of neural crest-derived mesenchyme and core mesoderm surrounded by pharyngeal epithelium. The mesenchyme needs to receive Hedgehog signaling for mandible development, but the epithelial tissue that signals to the mesenchyme has not been identified in mammals. Data presented in Chapter 2 show that Sonic Hedgehog is necessary at two distinct stages of mandible development by using a tissue specific genetic ablation to remove Sonic Hedgehog from the pharyngeal endoderm. First, we show that Sonic Hedgehog promotes cell survival prior to cartilage differentiation through immunostaining for Caspase-9, an apoptosis marker. Second, a rescue of early cell death with the p53 inhibitor pifithrin-α shows that Sonic Hedgehog is necessary for cartilage condensation and differentiation later in development. Without cartilage differentiation the mandible is unable to elongate properly and hypoplasia occurs.

Caudal to the pharyngeal epithelium is the anterior FGE, which develops into the larynx, esophagus and trachea. The anterior FGE is a single endodermal tube at E9.5 and by E11.5 compartmentalizes into two distinct tubes: the esophagus and trachea. While the signaling pathways involved in proper compartmentalization of the foregut are well studied, nothing is known about the cellular behaviors that drive this complex event. One important event during foregut compartmentalization is the establishment of dorso-ventral patterning, which is necessary for separation to occur. To elucidate the importance of dorso-ventral patterning, we take advantage of two genetic mouse models with disrupted patterning, an activation of and a removal of β-catenin in the ventral foregut endoderm. Data presented in Chapter 3 show that β-catenin is important for epithelial pseudostratification and the establishment of a region of double-positive cells at the dorso-ventral midline through close examination of epithelial morphogenesis at E10.5 prior to compartmentalization. This data has established two mouse models for studying changes in epithelial morphology during foregut compartmentalization. In total, this body of work details how signals originating in the pharyngeal and anterior foregut epithelium regulate both mesenchymal and epithelial behaviors during mandible and foregut development.


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9

Gruda, Agron [Verfasser]. "Herkömmliche, modifizierte und neue Messmethoden zur kephalometrischen Untersuchung der pränatalen craniofacialen Morphogenese des Menschen anhand von bilateralen und frontalen Darstellungen von 3D-Rekonstruktionen und von Aufhellungspräparaten menschlicher Embryonen und Föten von 19 mm SSL bis 145 mm SSL / von Agron Gruda." 2010. http://d-nb.info/1010554476/34.

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Книги з теми "Craniofacial morphogenesis"

1

E, Moyers Robert, Vig Katherine W. L, Burdi Alphonse R, and Ferrara Andrea M, eds. Craniofacial morphogenesis and dysmorphogenesis. Ann Arbor, Mich: Center for Human Growth and Development, University of Michigan, 1988.

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2

Kawakami, Toshiyuki. Cell differentiation of neoplastic cells originating in the oral and craniofacial regions. New York: Nova Science, 2008.

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3

E, Moyers Robert, Vig Katherine W. L, Burdi Alphonse R, and Ferrara Andrea M, eds. Craniofacial morphogenesis and dysmorphogenesis. Ann Arbor, Mich: Center for Human Growth and Development, University of Michigan, 1988.

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4

National Institute of Dental Research (U.S.), ed. Toward a Molecular Understanding of Craniofacial Morphogenesis. [S.l: s.n., 1998.

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Частини книг з теми "Craniofacial morphogenesis"

1

Rawlins, Joseph T., and Lynne A. Opperman. "Tgf-&Bg;; Regulation of Suture Morphogenesis and Growth." In Craniofacial Sutures, 178–96. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000115038.

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2

Jussila, Maria, Emma Juuri, and Irma Thesleff. "Tooth Morphogenesis and Renewal." In Stem Cells in Craniofacial Development and Regeneration, 109–34. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118498026.ch6.

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3

Trainor, Paul A. "Molecular Blueprint for Craniofacial Morphogenesis and Development." In Stem Cells in Craniofacial Development and Regeneration, 1–29. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118498026.ch1.

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Katsube, Motoki. "Morphometric Analysis for the Morphogenesis of the Craniofacial Structures and the Evolution of the Nasal Protrusion in Humans." In Multidisciplinary Computational Anatomy, 247–52. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-4325-5_32.

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Mishina, Yuji, and Nobuhiro Kamiya. "Embryonic Skeletogenesis and Craniofacial Development." In Bone Morphogenetic Proteins: Systems Biology Regulators, 39–72. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47507-3_3.

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6

Terheyden, Hendrik, and Søren Jepsen. "Craniofacial reconstruction with bone morphogenetic proteins." In Bone Morphogenetic Proteins: Regeneration of Bone and Beyond, 133–55. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7857-9_6.

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Lavelle, Christopher L. B. "Craniofacial morphogenesis." In Applied Oral Physiology, 176–82. Elsevier, 1988. http://dx.doi.org/10.1016/b978-0-7236-0818-9.50023-6.

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8

Merlo, Giorgio R., Annemiek Beverdam, and Giovanni Levi. "Dlx genes in craniofacial and limb morphogenesis">Dlx genes in craniofacial and limb morphogenesis." In Murine Homeobox Gene Control of Embryonic Patterning and Organogenesis, 107–32. Elsevier, 2003. http://dx.doi.org/10.1016/s1569-1799(03)13004-3.

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9

Dudas, Marek, and Vesa Kaartinen. "TGF-β Superfamily and Mouse Craniofacial Development: Interplay of Morphogenetic Proteins and Receptor Signaling Controls Normal Formation of the Face." In Current Topics in Developmental Biology, 65–133. Elsevier, 2005. http://dx.doi.org/10.1016/s0070-2153(05)66003-6.

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