The Experts below are selected from a list of 8880 Experts worldwide ranked by ideXlab platform
Yang Chai - One of the best experts on this subject based on the ideXlab platform.
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Msx1 and Dlx5 function synergistically to regulate Frontal Bone development.
genesis, 2010Co-Authors: Il Hyuk Chung, Jun Han, Junichi Iwata, Yang ChaiAbstract:The Msx and Dlx families of homeobox proteins are important regulators for embryogenesis. Loss of Msx1 in mice results in multiple developmental defects including craniofacial malformations. Although Dlx5 is widely expressed during embryonic development, targeted null mutation of Dlx5 mainly affects the development of craniofacial Bones. Msx1 and Dlx5 show overlapping expression patterns during Frontal Bone development. To investigate the functional significance of Msx1/Dlx5 interaction in regulating Frontal Bone development, we generated Msx1 and Dlx5 double null mutant mice. In Msx1−/−;Dlx5−/− mice, the Frontal Bones defect was more severe than that of either Msx1−/− or Dlx5−/− mice. This aggravated Frontal Bone defect suggests that Msx1 and Dlx5 function synergistically to regulate osteogenesis. This synergistic effect of Msx1 and Dlx5 on the Frontal Bone represents a tissue specific mode of interaction of the Msx and Dlx genes. Furthermore, Dlx5 requires Msx1 for its expression in the context of Frontal Bone development. Our study shows that Msx1/Dlx5 interaction is crucial for osteogenic induction during Frontal Bone development. genesis 48:645–655, 2010. © 2010 Wiley-Liss, Inc.
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Concerted action of Msx1 and Msx2 in regulating cranial neural crest cell differentiation during Frontal Bone development.
Mechanisms of development, 2007Co-Authors: Jun Han, Mamoru Ishii, Pablo Bringas, Richard L Maas, Robert E Maxson, Yang ChaiAbstract:The homeobox genes Msx1 and Msx2 function as transcriptional regulators that control cellular proliferation and differentiation during embryonic development. Mutations in the Msx1 and Msx2 genes in mice disrupt tissue-tissue interactions and cause multiple craniofacial malformations. Although Msx1 and Msx2 are both expressed throughout the entire development of the Frontal Bone, the Frontal Bone defect in Msx1 or Msx2 null mutants is rather mild, suggesting the possibility of functional compensation between Msx1 and Msx2 during early Frontal Bone development. To investigate this hypothesis, we generated Msx1(-/-);Msx2(-/-) mice. These double mutant embryos died at E17 to E18 with no formation of the Frontal Bone. There was no apparent defect in CNC migration into the presumptive Frontal Bone primordium, but differentiation of the Frontal mesenchyme and establishment of the Frontal primordium was defective, indicating that Msx1 and Msx2 genes are specifically required for osteogenesis in the cranial neural crest lineage within the Frontal Bone primordium. Mechanistically, our data suggest that Msx genes are critical for the expression of Runx2 in the frontonasal subpopulation of cranial neural crest cells and for differentiation of the osteogenic lineage. This early function of the Msx genes is likely independent of the Bmp signaling pathway.
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tgfβ mediated fgf signaling is crucial for regulating cranial neural crest cell proliferation during Frontal Bone development
Development, 2005Co-Authors: Tomoyo Sasaki, Pablo Bringas, Yoshihiro Ito, Stanley Chou, Mark M Urata, Harold C Slavkin, Yang ChaiAbstract:The murine Frontal Bone derives entirely from the cranial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the Frontal lobe of brain and the orbital aspect that forms the roof of bony orbit. TGFbeta and FGF signaling have important regulatory roles in postnatal calvarial development. Our previous study has demonstrated that conditional inactivation of Tgfbr2 in the neural crest results in severe defects in calvarial development, although the cellular and molecular mechanisms by which TGFbeta signaling regulates the fate of CNC cells during Frontal Bone development remain unknown. Here, we show that TGFbeta IIR is required for proliferation of osteoprogenitor cells in the CNC-derived Frontal Bone anlagen. FGF acts downstream of TGFbeta signaling in regulating CNC cell proliferation, and exogenous FGF2 rescues the cell proliferation defect in the Frontal primordium of Tgfbr2 mutant. Furthermore, the CNC-derived Frontal primordium requires TGFbeta IIR to undergo terminal differentiation. However, this requirement is restricted to the developing calvarial aspect of the Frontal Bone, whereas the orbital aspect forms despite the ablation of Tgfbr2 gene, implying a differential requirement for TGFbeta signaling during the development of various regions of the Frontal Bone. This study demonstrates the biological significance of TGFbeta-mediated FGF signaling cascade in regulating Frontal Bone development, suggests that TGFbeta functions as a morphogen in regulating the fate of the CNC-derived osteoblast and provides a model for investigating abnormal craniofacial development.
Jun Han - One of the best experts on this subject based on the ideXlab platform.
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Msx1 and Dlx5 function synergistically to regulate Frontal Bone development.
genesis, 2010Co-Authors: Il Hyuk Chung, Jun Han, Junichi Iwata, Yang ChaiAbstract:The Msx and Dlx families of homeobox proteins are important regulators for embryogenesis. Loss of Msx1 in mice results in multiple developmental defects including craniofacial malformations. Although Dlx5 is widely expressed during embryonic development, targeted null mutation of Dlx5 mainly affects the development of craniofacial Bones. Msx1 and Dlx5 show overlapping expression patterns during Frontal Bone development. To investigate the functional significance of Msx1/Dlx5 interaction in regulating Frontal Bone development, we generated Msx1 and Dlx5 double null mutant mice. In Msx1−/−;Dlx5−/− mice, the Frontal Bones defect was more severe than that of either Msx1−/− or Dlx5−/− mice. This aggravated Frontal Bone defect suggests that Msx1 and Dlx5 function synergistically to regulate osteogenesis. This synergistic effect of Msx1 and Dlx5 on the Frontal Bone represents a tissue specific mode of interaction of the Msx and Dlx genes. Furthermore, Dlx5 requires Msx1 for its expression in the context of Frontal Bone development. Our study shows that Msx1/Dlx5 interaction is crucial for osteogenic induction during Frontal Bone development. genesis 48:645–655, 2010. © 2010 Wiley-Liss, Inc.
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Concerted action of Msx1 and Msx2 in regulating cranial neural crest cell differentiation during Frontal Bone development.
Mechanisms of development, 2007Co-Authors: Jun Han, Mamoru Ishii, Pablo Bringas, Richard L Maas, Robert E Maxson, Yang ChaiAbstract:The homeobox genes Msx1 and Msx2 function as transcriptional regulators that control cellular proliferation and differentiation during embryonic development. Mutations in the Msx1 and Msx2 genes in mice disrupt tissue-tissue interactions and cause multiple craniofacial malformations. Although Msx1 and Msx2 are both expressed throughout the entire development of the Frontal Bone, the Frontal Bone defect in Msx1 or Msx2 null mutants is rather mild, suggesting the possibility of functional compensation between Msx1 and Msx2 during early Frontal Bone development. To investigate this hypothesis, we generated Msx1(-/-);Msx2(-/-) mice. These double mutant embryos died at E17 to E18 with no formation of the Frontal Bone. There was no apparent defect in CNC migration into the presumptive Frontal Bone primordium, but differentiation of the Frontal mesenchyme and establishment of the Frontal primordium was defective, indicating that Msx1 and Msx2 genes are specifically required for osteogenesis in the cranial neural crest lineage within the Frontal Bone primordium. Mechanistically, our data suggest that Msx genes are critical for the expression of Runx2 in the frontonasal subpopulation of cranial neural crest cells and for differentiation of the osteogenic lineage. This early function of the Msx genes is likely independent of the Bmp signaling pathway.
Pablo Bringas - One of the best experts on this subject based on the ideXlab platform.
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Concerted action of Msx1 and Msx2 in regulating cranial neural crest cell differentiation during Frontal Bone development.
Mechanisms of development, 2007Co-Authors: Jun Han, Mamoru Ishii, Pablo Bringas, Richard L Maas, Robert E Maxson, Yang ChaiAbstract:The homeobox genes Msx1 and Msx2 function as transcriptional regulators that control cellular proliferation and differentiation during embryonic development. Mutations in the Msx1 and Msx2 genes in mice disrupt tissue-tissue interactions and cause multiple craniofacial malformations. Although Msx1 and Msx2 are both expressed throughout the entire development of the Frontal Bone, the Frontal Bone defect in Msx1 or Msx2 null mutants is rather mild, suggesting the possibility of functional compensation between Msx1 and Msx2 during early Frontal Bone development. To investigate this hypothesis, we generated Msx1(-/-);Msx2(-/-) mice. These double mutant embryos died at E17 to E18 with no formation of the Frontal Bone. There was no apparent defect in CNC migration into the presumptive Frontal Bone primordium, but differentiation of the Frontal mesenchyme and establishment of the Frontal primordium was defective, indicating that Msx1 and Msx2 genes are specifically required for osteogenesis in the cranial neural crest lineage within the Frontal Bone primordium. Mechanistically, our data suggest that Msx genes are critical for the expression of Runx2 in the frontonasal subpopulation of cranial neural crest cells and for differentiation of the osteogenic lineage. This early function of the Msx genes is likely independent of the Bmp signaling pathway.
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tgfβ mediated fgf signaling is crucial for regulating cranial neural crest cell proliferation during Frontal Bone development
Development, 2005Co-Authors: Tomoyo Sasaki, Pablo Bringas, Yoshihiro Ito, Stanley Chou, Mark M Urata, Harold C Slavkin, Yang ChaiAbstract:The murine Frontal Bone derives entirely from the cranial neural crest (CNC) and consists of the calvarial (lateral) aspect that covers the Frontal lobe of brain and the orbital aspect that forms the roof of bony orbit. TGFbeta and FGF signaling have important regulatory roles in postnatal calvarial development. Our previous study has demonstrated that conditional inactivation of Tgfbr2 in the neural crest results in severe defects in calvarial development, although the cellular and molecular mechanisms by which TGFbeta signaling regulates the fate of CNC cells during Frontal Bone development remain unknown. Here, we show that TGFbeta IIR is required for proliferation of osteoprogenitor cells in the CNC-derived Frontal Bone anlagen. FGF acts downstream of TGFbeta signaling in regulating CNC cell proliferation, and exogenous FGF2 rescues the cell proliferation defect in the Frontal primordium of Tgfbr2 mutant. Furthermore, the CNC-derived Frontal primordium requires TGFbeta IIR to undergo terminal differentiation. However, this requirement is restricted to the developing calvarial aspect of the Frontal Bone, whereas the orbital aspect forms despite the ablation of Tgfbr2 gene, implying a differential requirement for TGFbeta signaling during the development of various regions of the Frontal Bone. This study demonstrates the biological significance of TGFbeta-mediated FGF signaling cascade in regulating Frontal Bone development, suggests that TGFbeta functions as a morphogen in regulating the fate of the CNC-derived osteoblast and provides a model for investigating abnormal craniofacial development.
Sheela Athreya - One of the best experts on this subject based on the ideXlab platform.
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The Frontal Bone in the genus Homo: a survey of functional and phylogenetic sources of variation.
Journal of anthropological sciences = Rivista di antropologia : JASS, 2012Co-Authors: Sheela AthreyaAbstract:The Frontal Bone is a useful aspect of the craniofacial skeleton to study in physical anthropology because it contains several characters considered to be important for both population- and species-level distinctions. These include forehead (Frontal squama) inclination and supraorbital morphology. Because it lies at the interface between the anterior neurocranium and the upper face, it is also informative about the evolution of both of these regions of the skull. Previous research on Frontal Bone morphology can be grouped into two broad categories. One set of studies explored the relationship between craniofacial structure and function in an attempt to explain biological sources of variation in the torus development of various extant primate species, including modern humans. The second group of studies examined geographical and temporal patterns of variation in Frontal morphology to make inferences about the phylogenetic relationship relationships among fossil hominin populations in the Pleistocene. This paper offers a review of both phylogenetic and functional studies of variation in Frontal Bone morphology, and synthesizes them to offer a comprehensive understanding of what the Frontal Bone can tell us about bio-behavioral and evolutionary differences both among extant and extinct members of the genus Homo.
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a comparative study of Frontal Bone morphology among pleistocene hominin fossil groups
Journal of Human Evolution, 2009Co-Authors: Sheela AthreyaAbstract:Features of the Frontal Bone that are conventionally used to distinguish among fossil hominin groups were quantitatively examined. Fifty-five fossil crania dating from the early to the late Pleistocene were analyzed. Using a modified pantograph, outlines of the Frontal Bone were collected along the midsagittal and two parasagittal planes. The profile from nasion to bregma, as well as two profiles above the medial and lateral sections of the orbit, respectively, extending from the orbital margin to the coronal suture were traced. The outlines were measured using Elliptical Fourier Function Analysis (EFFA), which enabled a quantification of aspects of the Frontal Bone that have historically been described primarily in nonmetric or linear terms. Four measurements were obtained: 1) overall morphology as expressed in the Fourier harmonic amplitudes; 2) maximum projection of the supraorbital torus at three points along the browridge (glabella and the medial and lateral aspects of the torus above the orbit); 3) maximum distance of the Frontal squama from the Frontal chord, capturing forehead curvature; and 4) nasion-bregma chord length. The results indicate that the midsagittal profile is significantly different among all Pleistocene groups in analyses that include both size and shape, as well as size-adjusted data. Homo erectus is significantly different from the late Pleistocene groups (Neandertals and early modern H. sapiens) in glabellar projection. Anatomically modern humans are significantly different from all other groups in both raw and size-standardized analyses of all three outlines that captured overall morphology, as well as forehead curvature and lateral supraorbital torus prominence, and middle Pleistocene Homo are significantly different in both medial and lateral overall parasagittal form. However, for the majority of analyses there were no significant differences among the Pleistocene archaic groups in supraorbital torus projection, Frontal squama curvature, nasion-bregma chord length, or overall Frontal Bone morphology.
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Patterning of geographic variation in Middle Pleistocene Homo Frontal Bone morphology.
Journal of human evolution, 2006Co-Authors: Sheela AthreyaAbstract:A quantitative assessment of the Frontal Bone morphology of a sample of Middle Pleistocene hominins was undertaken in order to address questions regarding their population structure and evolutionary history. Outline tracings of the Frontal Bones of forty-seven fossil crania were obtained, and size-standardized measurements were then computed using an Elliptical Fourier analysis of these tracings. Principal component scores of the Fourier harmonic amplitudes were derived and served as a quantitative representation of the morphology of the Frontal Bone. Morphological, geographical, and temporal distance matrices were then constructed between each pair of fossils. A partial Mantel matrix correlation test was performed between morphological and geographical distance matrices, controlling for temporal distance, in order to determine if the pattern of geographical differentiation in features of the Frontal Bone of mid-Pleistocene Homo followed that of an isolation-by-distance model of population structure. The results of the partial Mantel tests indicate that the overall patterning of differentiation in the features of the Frontal Bone cannot best be explained by a population structure shaped by isolation-by-distance. Additionally, various aspects of the Frontal Bone quantified here follow different patterns of geographical differentiation, suggesting that a mosaic pattern of evolution holds true for characters within one cranial region and not just for those between regions.
Mamoru Ishii - One of the best experts on this subject based on the ideXlab platform.
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Concerted action of Msx1 and Msx2 in regulating cranial neural crest cell differentiation during Frontal Bone development.
Mechanisms of development, 2007Co-Authors: Jun Han, Mamoru Ishii, Pablo Bringas, Richard L Maas, Robert E Maxson, Yang ChaiAbstract:The homeobox genes Msx1 and Msx2 function as transcriptional regulators that control cellular proliferation and differentiation during embryonic development. Mutations in the Msx1 and Msx2 genes in mice disrupt tissue-tissue interactions and cause multiple craniofacial malformations. Although Msx1 and Msx2 are both expressed throughout the entire development of the Frontal Bone, the Frontal Bone defect in Msx1 or Msx2 null mutants is rather mild, suggesting the possibility of functional compensation between Msx1 and Msx2 during early Frontal Bone development. To investigate this hypothesis, we generated Msx1(-/-);Msx2(-/-) mice. These double mutant embryos died at E17 to E18 with no formation of the Frontal Bone. There was no apparent defect in CNC migration into the presumptive Frontal Bone primordium, but differentiation of the Frontal mesenchyme and establishment of the Frontal primordium was defective, indicating that Msx1 and Msx2 genes are specifically required for osteogenesis in the cranial neural crest lineage within the Frontal Bone primordium. Mechanistically, our data suggest that Msx genes are critical for the expression of Runx2 in the frontonasal subpopulation of cranial neural crest cells and for differentiation of the osteogenic lineage. This early function of the Msx genes is likely independent of the Bmp signaling pathway.
