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  1. Article ; Online: The evolution of human artistic creativity.

    Morriss-Kay, Gillian M

    Journal of anatomy

    2009  Volume 216, Issue 2, Page(s) 158–176

    Abstract: Creating visual art is one of the defining characteristics of the human species, but the paucity of archaeological evidence means that we have limited information on the origin and evolution of this aspect of human culture. The components of art include ... ...

    Abstract Creating visual art is one of the defining characteristics of the human species, but the paucity of archaeological evidence means that we have limited information on the origin and evolution of this aspect of human culture. The components of art include colour, pattern and the reproduction of visual likeness. The 2D and 3D art forms that were created by Upper Palaeolithic Europeans at least 30,000 years ago are conceptually equivalent to those created in recent centuries, indicating that human cognition and symbolling activity, as well as anatomy, were fully modern by that time. The origins of art are therefore much more ancient and lie within Africa, before worldwide human dispersal. The earliest known evidence of 'artistic behaviour' is of human body decoration, including skin colouring with ochre and the use of beads, although both may have had functional origins. Zig-zag and criss-cross patterns, nested curves and parallel lines are the earliest known patterns to have been created separately from the body; their similarity to entopic phenomena (involuntary products of the visual system) suggests a physiological origin. 3D art may have begun with human likeness recognition in natural objects, which were modified to enhance that likeness; some 2D art has also clearly been influenced by suggestive features of an uneven surface. The creation of images from the imagination, or 'the mind's eye', required a seminal evolutionary change in the neural structures underpinning perception; this change would have had a survival advantage in both tool-making and hunting. Analysis of early tool-making techniques suggests that creating 3D objects (sculptures and reliefs) involves their cognitive deconstruction into a series of surfaces, a principle that could have been applied to early sculpture. The cognitive ability to create art separate from the body must have originated in Africa but the practice may have begun at different times in genetically and culturally distinct groups both within Africa and during global dispersal, leading to the regional variety seen in both ancient and recent art. At all stages in the evolution of artistic creativity, stylistic change must have been due to rare, highly gifted individuals.
    MeSH term(s) Anatomy/history ; Animals ; Archaeology/history ; Art/history ; Creativity ; Cultural Evolution/history ; History, Ancient ; Human Body ; Humans
    Language English
    Publishing date 2009-11-09
    Publishing country England
    Document type Historical Article ; Journal Article ; Review
    ZDB-ID 2955-5
    ISSN 1469-7580 ; 0021-8782
    ISSN (online) 1469-7580
    ISSN 0021-8782
    DOI 10.1111/j.1469-7580.2009.01160.x
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  2. Article: Treatment of mice with retinoids in vivo and in vitro.

    Morriss-Kay, Gillian M

    Methods in molecular biology (Clifton, N.J.)

    2008  Volume 461, Page(s) 31–36

    MeSH term(s) Animals ; Brain Diseases/chemically induced ; Brain Diseases/congenital ; Brain Diseases/pathology ; Cell Culture Techniques/methods ; Drug Evaluation, Preclinical/methods ; Embryo, Mammalian/drug effects ; Injections, Intraperitoneal ; Limb Deformities, Congenital/chemically induced ; Mice/metabolism ; Mice/physiology ; Models, Animal ; Retinoids/administration & dosage ; Retinoids/pharmacology ; Rhombencephalon/abnormalities
    Chemical Substances Retinoids
    Language English
    Publishing date 2008
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 1064-3745
    ISSN 1064-3745
    DOI 10.1007/978-1-60327-483-8_4
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  3. Article: Growth of the normal skull vault and its alteration in craniosynostosis: insights from human genetics and experimental studies.

    Morriss-Kay, Gillian M / Wilkie, Andrew O M

    Journal of anatomy

    2005  Volume 207, Issue 5, Page(s) 637–653

    Abstract: The mammalian skull vault is constructed principally from five bones: the paired frontals and parietals, and the unpaired interparietal. These bones abut at sutures, where most growth of the skull vault takes place. Sutural growth involves maintenance of ...

    Abstract The mammalian skull vault is constructed principally from five bones: the paired frontals and parietals, and the unpaired interparietal. These bones abut at sutures, where most growth of the skull vault takes place. Sutural growth involves maintenance of a population of proliferating osteoprogenitor cells which differentiate into bone matrix-secreting osteoblasts. Sustained function of the sutures as growth centres is essential for continuous expansion of the skull vault to accommodate the growing brain. Craniosynostosis, the premature fusion of the cranial sutures, occurs in 1 in 2500 children and often presents challenging clinical problems. Until a dozen years ago, little was known about the causes of craniosynostosis but the discovery of mutations in the MSX2, FGFR1, FGFR2, FGFR3, TWIST1 and EFNB1 genes in both syndromic and non-syndromic cases has led to considerable insights into the aetiology, classification and developmental pathology of these disorders. Investigations of the biological roles of these genes in cranial development and growth have been carried out in normal and mutant mice, elucidating their individual and interdependent roles in normal sutures and in sutures undergoing synostosis. Mouse studies have also revealed a significant correspondence between the neural crest-mesoderm boundary in the early embryonic head and the position of cranial sutures, suggesting roles for tissue interaction in suture formation, including initiation of the signalling system that characterizes the functionally active suture.
    MeSH term(s) Animals ; Cranial Sutures/embryology ; Craniosynostoses/embryology ; Fetal Development/genetics ; Gene Expression Regulation, Developmental ; Genes, Homeobox ; Humans ; Mice ; Mice, Mutant Strains ; Morphogenesis/genetics ; Mutation ; Skull/embryology
    Language English
    Publishing date 2005-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2955-5
    ISSN 1469-7580 ; 0021-8782
    ISSN (online) 1469-7580
    ISSN 0021-8782
    DOI 10.1111/j.1469-7580.2005.00475.x
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  4. Article ; Online: Polydactyly in the mouse mutant Doublefoot involves altered Gli3 processing and is caused by a large deletion in cis to Indian hedgehog.

    Babbs, Christian / Furniss, Dominic / Morriss-Kay, Gillian M / Wilkie, Andrew O M

    Mechanisms of development

    2008  Volume 125, Issue 5-6, Page(s) 517–526

    Abstract: The mouse mutant Doublefoot (Dbf) shows preaxial polydactyly with 6-9 triphalangeal digits in all four limbs and additional abnormalities including a broadened skull, hydrocephalus, and a thickened, kinked tail. The autopod undergoes a characteristic ... ...

    Abstract The mouse mutant Doublefoot (Dbf) shows preaxial polydactyly with 6-9 triphalangeal digits in all four limbs and additional abnormalities including a broadened skull, hydrocephalus, and a thickened, kinked tail. The autopod undergoes a characteristic expansion between late embryonic day (E) 10.5 and E11.5, following the onset of ectopic Indian hedgehog (Ihh) expression in the entire distal mesenchyme, except for the zone of polarising activity (ZPA), at E10.5. We show here that limb prepattern, as indicated by expression of Gli3 and Hand2 at E9.5 is unaffected by the mutation. As both Sonic hedgehog (Shh) and Ihh expression are present in Dbf limb buds at E10.5, we generated Dbf/(+);Shh(-/-) mutants to analyse the effects of different patterns of Hedgehog activity on the limb phenotype and molecular differentiation. Dbf/(+) embryos lacking Shh showed postaxial as well as preaxial polydactyly, and the Ihh expression domain extended posteriorly into the domain in which Shh is normally expressed, indicating loss of ZPA identity. Differences in gene expression patterns in wild type, single and compound mutants were associated with differences in Gli3 processing: an increased ratio of Gli3 activator to Gli3 repressor was observed in the anterior half of Dbf/(+) limb buds and in both anterior and posterior halves of compound mutant limb buds at E10.5. To identify the cause of Ihh misregulation in Dbf/(+) mutants, we sequenced approximately 20 kb of genomic DNA around Ihh but found no pathogenic changes. However, Southern blot analysis revealed a approximately 600 kb deletion disrupting or deleting 25 transcripts, starting 50 kb 5' of Ihh and extending away from the gene. The large deletion interval may explain the wide range of abnormalities in Dbf/(+) mutants. However, we did not detect anologous deletions in cases of Laurin-Sandrow syndrome, a human disorder that shows phenotypic similarities to Dbf.
    MeSH term(s) Animals ; Base Sequence ; Body Patterning ; Extremities ; Gene Deletion ; Gene Expression Regulation, Developmental ; Hedgehog Proteins/genetics ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/physiology ; Mice ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/physiology ; Polydactyly/genetics ; Sequence Homology, Nucleic Acid ; Time Factors ; Zinc Finger Protein Gli3
    Chemical Substances Gli3 protein, mouse ; Hedgehog Proteins ; Kruppel-Like Transcription Factors ; Nerve Tissue Proteins ; Shh protein, mouse ; Zinc Finger Protein Gli3 ; ihh protein, mouse
    Language English
    Publishing date 2008-01-11
    Publishing country Ireland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1055986-3
    ISSN 1872-6356 ; 0925-4773
    ISSN (online) 1872-6356
    ISSN 0925-4773
    DOI 10.1016/j.mod.2008.01.001
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  5. Article ; Online: Mechanism of skull suture maintenance and interdigitation.

    Miura, Takashi / Perlyn, Chad A / Kinboshi, Masato / Ogihara, Naomichi / Kobayashi-Miura, Mikiko / Morriss-Kay, Gillian M / Shiota, Kohei

    Journal of anatomy

    2009  Volume 215, Issue 6, Page(s) 642–655

    Abstract: Skull sutures serve as growth centers whose function involves multiple molecular pathways. During periods of brain growth the sutures remain thin and straight, later developing complex fractal interdigitations that provide interlocking strength. The ... ...

    Abstract Skull sutures serve as growth centers whose function involves multiple molecular pathways. During periods of brain growth the sutures remain thin and straight, later developing complex fractal interdigitations that provide interlocking strength. The nature of the relationship between the molecular interactions and suture pattern formation is not understood. Here we show that by classifying the molecules involved into two groups, stabilizing factors and substrate molecules, complex molecular networks can be modeled by a simple two-species reaction-diffusion model that recapitulates all the known behavior of suture pattern formation. This model reproduces the maintenance of thin sutural tissue at early stages, the later modification of the straight suture to form osseous interdigitations, and the formation of fractal structures. Predictions from the model are in good agreement with experimental observations, indicating that the model captures the essential nature of the interdigitation process.
    MeSH term(s) Aging/pathology ; Aging/physiology ; Animals ; Cranial Sutures/anatomy & histology ; Cranial Sutures/growth & development ; Cranial Sutures/physiology ; Fractals ; Humans ; Mice ; Mice, Inbred ICR ; Models, Biological ; Organ Culture Techniques ; Osteogenesis/physiology ; Reverse Transcriptase Polymerase Chain Reaction/methods
    Language English
    Publishing date 2009-10-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2955-5
    ISSN 1469-7580 ; 0021-8782
    ISSN (online) 1469-7580
    ISSN 0021-8782
    DOI 10.1111/j.1469-7580.2009.01148.x
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  6. Article ; Online: A model for the pharmacological treatment of crouzon syndrome.

    Perlyn, Chad A / Morriss-Kay, Gillian / Darvann, Tron / Tenenbaum, Marissa / Ornitz, David M

    Neurosurgery

    2006  Volume 59, Issue 1, Page(s) 210–5; discussion 210–5

    Abstract: Objective: Crouzon syndrome is caused by mutations in fibroblast growth factor receptor 2 (FGFR2) leading to constitutive activation of receptors in the absence of ligand binding. The syndrome is characterized by premature fusion of the cranial sutures ... ...

    Abstract Objective: Crouzon syndrome is caused by mutations in fibroblast growth factor receptor 2 (FGFR2) leading to constitutive activation of receptors in the absence of ligand binding. The syndrome is characterized by premature fusion of the cranial sutures that leads to abnormal cranium shape, restricted brain growth, and increased intracranial pressure. Surgical remodeling of the cranial vault is currently used to treat affected infants. The purpose of this study was to develop a pharmacological strategy using tyrosine kinase inhibition as a novel treatment for craniosynostotic syndromes caused by constitutive FGFR activation.
    Methods: Characterization of cranial suture fusion in Fgfr2 mutant mice, which carry the most common Crouzon mutation, was performed using micro-computed tomographic analysis from embryogenesis through maturation. Whole calvarial cultures from wild-type and Fgfr2 mice were established and cultured for 2 weeks in the presence of dimethyl sulfoxide control or PD173074, an FGFR tyrosine kinase inhibitor. Paraffin sections were prepared to show suture morphology and calcium deposition.
    Results: In untreated Fgfr2 cultures, the coronal suture fused bilaterally with loss of overlap between the frontal bone and parietal bone. Calvaria treated with PD173074 (2 micromol/L) showed patency of the coronal suture and were without evidence of any synostosis.
    Conclusion: We report the successful use of PD173074 to prevent in vitro suture fusion in a model for Crouzon syndrome. Further studies are underway to develop an in vivo treatment protocol as a novel therapeutic modality for FGFR associated craniosynostotic syndromes.
    MeSH term(s) Animals ; Cranial Sutures/diagnostic imaging ; Cranial Sutures/drug effects ; Cranial Sutures/embryology ; Cranial Sutures/physiopathology ; Craniofacial Dysostosis/diagnostic imaging ; Craniofacial Dysostosis/drug therapy ; Craniofacial Dysostosis/genetics ; Craniofacial Dysostosis/physiopathology ; Cysteine ; Disease Models, Animal ; Mice ; Mice, Mutant Strains ; Mutation ; Pyrimidines/therapeutic use ; Receptor, Fibroblast Growth Factor, Type 2/genetics ; Receptors, Fibroblast Growth Factor/antagonists & inhibitors ; Tissue Culture Techniques ; Tomography, X-Ray Computed ; Tyrosine
    Chemical Substances PD 173074 ; Pyrimidines ; Receptors, Fibroblast Growth Factor ; Tyrosine (42HK56048U) ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1) ; Cysteine (K848JZ4886)
    Language English
    Publishing date 2006-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 135446-2
    ISSN 1524-4040 ; 0148-396X
    ISSN (online) 1524-4040
    ISSN 0148-396X
    DOI 10.1227/01.NEU.0000224323.53866.1E
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  7. Article: Alx4 and Msx2 play phenotypically similar and additive roles in skull vault differentiation.

    Antonopoulou, Ileana / Mavrogiannis, Lampros A / Wilkie, Andrew O M / Morriss-Kay, Gillian M

    Journal of anatomy

    2004  Volume 204, Issue 6, Page(s) 487–499

    Abstract: Alx4 and Msx2 encode homeodomain-containing transcription factors that show a clear functional overlap. In both mice and humans, loss of function of either gene is associated with ossification defects of the skull vault, although the major effect is on ... ...

    Abstract Alx4 and Msx2 encode homeodomain-containing transcription factors that show a clear functional overlap. In both mice and humans, loss of function of either gene is associated with ossification defects of the skull vault, although the major effect is on the frontal bones in mice and the parietal bones in humans. This study was undertaken to discover whether Alx4 and Msx2 show a genetic interaction in skull vault ossification, and to test the hypothesis that they interact with the pathway that includes the Fgfr genes, Twist1 and Runx2. We generated Alx4(+/-)/Msx2(+/-) double heterozygous mutant mice, interbred them to produce compound genotypes and analysed the genotype-phenotype relationships. Loss of an increasing number of alleles correlated with an incremental exacerbation of the skull vault defect; loss of Alx4 function had a marginally greater effect than loss of Msx2 and also affected skull thickness. In situ hybridization showed that Alx4 and Msx2 are expressed in the cranial skeletogenic mesenchyme and in the growing calvarial bones. Studies of the coronal suture region at embryonic day (E)16.5 revealed that Alx4 expression was decreased, but not abolished, in Msx2(-/-) mutants, and vice versa; expression of Fgfr2 and Fgfr1, but not Twist1, was reduced in both mutants at the same stage. Runx2 expression was unaffected in the coronal suture; in contrast, expression of the downstream ossification marker Spp1 was delayed. Double homozygous pups showed substantial reduction of alkaline phosphatase expression throughout the mineralized skull vault; they died at birth due to defects of the heart, lungs and diaphragm not previously associated with Alx4 or Msx2. Our observations suggest that Alx4 and Msx2 are partially functionally redundant, acting within a network of transcription factors and signalling events that regulate the rate of osteogenic proliferation and differentiation at a stage after the commitment of mesenchymal stem cells to osteogenesis.
    MeSH term(s) Animals ; Animals, Newborn ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/physiology ; Embryonic and Fetal Development/physiology ; Gene Expression ; Genotype ; Homeodomain Proteins ; In Situ Hybridization ; Mice ; Mice, Inbred BALB C ; Mice, Mutant Strains ; Osteogenesis/physiology ; Phenotype ; Skull/embryology ; Skull/metabolism ; Transcription Factors/genetics ; Transcription Factors/physiology
    Chemical Substances ALX4 protein, human ; DNA-Binding Proteins ; Homeodomain Proteins ; MSX2 protein ; Transcription Factors
    Language English
    Publishing date 2004-06
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2955-5
    ISSN 1469-7580 ; 0021-8782
    ISSN (online) 1469-7580
    ISSN 0021-8782
    DOI 10.1111/j.0021-8782.2004.00304.x
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  8. Article: A gain-of-function mutation of Fgfr2c demonstrates the roles of this receptor variant in osteogenesis.

    Eswarakumar, Veraragavan P / Horowitz, Mark C / Locklin, Rachel / Morriss-Kay, Gillian M / Lonai, Peter

    Proceedings of the National Academy of Sciences of the United States of America

    2004  Volume 101, Issue 34, Page(s) 12555–12560

    Abstract: The b and c variants of fibroblast growth factor receptor 2 (FGFR2) differ in sequence, binding specificity, and localization. Fgfr2b, expressed in epithelia, is required for limb outgrowth and branching morphogenesis, whereas the mesenchymal Fgfr2c ... ...

    Abstract The b and c variants of fibroblast growth factor receptor 2 (FGFR2) differ in sequence, binding specificity, and localization. Fgfr2b, expressed in epithelia, is required for limb outgrowth and branching morphogenesis, whereas the mesenchymal Fgfr2c variant is required by the osteocyte lineage for normal skeletogenesis. Gain-of-function mutations in human FGFR2c are associated with craniosynostosis syndromes. To confirm and extend this evidence, we introduced a Cys342Tyr replacement into Fgfr2c to create a gain-of-function mutation equivalent to a mutation in human Crouzon and Pfeiffer syndromes. Fgfr2c(C342Y/)(+) heterozygote mice are viable and fertile with shortened face, protruding eyes, premature fusion of cranial sutures, and enhanced Spp1 expression in the calvaria. Homozygous mutants display multiple joint fusions, cleft palate, and trachea and lung defects, and die shortly after birth. They show enhanced Cbfa1/Runx2 expression without significant change in chondrocyte-specific Ihh, PTHrP, Sox9, Col2a, or Col10a gene expression. Histomorphometric analysis and bone marrow stromal cell culture showed a significant increase of osteoblast progenitors with no change in osteoclastogenic cells. Chondrocyte proliferation was decreased in the skull base at embryonic day 14.5 but not later. These results suggest that long-term aspects of the mutant phenotype, including craniosynostosis, are related to the Fgfr2c regulation of the osteoblast lineage. The effect on early chondrocyte proliferation but not gene expression suggests cooperation of Fgfr2c with Fgfr3 in the formation of the cartilage model for endochondral bone.
    MeSH term(s) Animals ; Bone and Bones/abnormalities ; Cell Division/physiology ; Core Binding Factor Alpha 1 Subunit ; Cranial Sutures/pathology ; Cranial Sutures/physiology ; Craniofacial Dysostosis/genetics ; Humans ; Lung/abnormalities ; Mice ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Osteogenesis/physiology ; Phenotype ; Point Mutation ; Receptor, Fibroblast Growth Factor, Type 2 ; Receptors, Fibroblast Growth Factor/genetics ; Receptors, Fibroblast Growth Factor/metabolism ; Skull/abnormalities ; Skull/anatomy & histology ; Skull/growth & development ; Skull/pathology ; Trachea/abnormalities ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Core Binding Factor Alpha 1 Subunit ; Neoplasm Proteins ; Receptors, Fibroblast Growth Factor ; Transcription Factors ; Receptor, Fibroblast Growth Factor, Type 2 (EC 2.7.10.1)
    Language English
    Publishing date 2004-08-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0405031101
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  9. Article: Developmental mechanisms underlying polydactyly in the mouse mutant Doublefoot.

    Crick, Alexandra P / Babbs, Christian / Brown, Jennifer M / Morriss-Kay, Gillian M

    Journal of anatomy

    2002  Volume 202, Issue 1, Page(s) 21–26

    Abstract: The pre-axial polydactylous mouse mutant Doublefoot has 6-9 digits per limb but lacks anteroposterior polarity (there is no biphalangeal digit 1). It differs from other polydactylous mutants in showing normal Shh expression, but polarizing activity ( ... ...

    Abstract The pre-axial polydactylous mouse mutant Doublefoot has 6-9 digits per limb but lacks anteroposterior polarity (there is no biphalangeal digit 1). It differs from other polydactylous mutants in showing normal Shh expression, but polarizing activity (shown by mouse-chick grafting experiments) and hedgehog signalling activity (shown by expression of Ptc1) are present throughout the distal mesenchyme. The Dbf mutation has not yet been identified. Here we review current understanding of this mutant, and briefly report new results indicating (1) that limb bud expansion is concomitant with ectopic lhh expression and with extension of the posterior high cell proliferation rate into the anterior region, and (2) that the Dbf mutation is epistatic to Shh in the limb.
    MeSH term(s) Animals ; Gene Expression ; Gene Expression Regulation, Developmental ; Hedgehog Proteins ; Limb Buds/physiology ; Mesoderm/physiology ; Mice ; Mice, Mutant Strains ; Models, Animal ; Morphogenesis/genetics ; Polydactyly/embryology ; Polydactyly/genetics ; Trans-Activators/genetics
    Chemical Substances Hedgehog Proteins ; Trans-Activators
    Language English
    Publishing date 2002-12-13
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2955-5
    ISSN 1469-7580 ; 0021-8782
    ISSN (online) 1469-7580
    ISSN 0021-8782
    DOI 10.1046/j.1469-7580.2003.00132.x
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  10. Article: Tissue origins and interactions in the mammalian skull vault.

    Jiang, Xiaobing / Iseki, Sachiko / Maxson, Robert E / Sucov, Henry M / Morriss-Kay, Gillian M

    Developmental biology

    2002  Volume 241, Issue 1, Page(s) 106–116

    Abstract: During mammalian evolution, expansion of the cerebral hemispheres was accompanied by expansion of the frontal and parietal bones of the skull vault and deployment of the coronal (fronto-parietal) and sagittal (parietal-parietal) sutures as major growth ... ...

    Abstract During mammalian evolution, expansion of the cerebral hemispheres was accompanied by expansion of the frontal and parietal bones of the skull vault and deployment of the coronal (fronto-parietal) and sagittal (parietal-parietal) sutures as major growth centres. Using a transgenic mouse with a permanent neural crest cell lineage marker, Wnt1-Cre/R26R, we show that both sutures are formed at a neural crest-mesoderm interface: the frontal bones are neural crest-derived and the parietal bones mesodermal, with a tongue of neural crest between the two parietal bones. By detailed analysis of neural crest migration pathways using X-gal staining, and mesodermal tracing by DiI labelling, we show that the neural crest-mesodermal tissue juxtaposition that later forms the coronal suture is established at E9.5 as the caudal boundary of the frontonasal mesenchyme. As the cerebral hemispheres expand, they extend caudally, passing beneath the neural crest-mesodermal interface within the dermis, carrying with them a layer of neural crest cells that forms their meningeal covering. Exposure of embryos to retinoic acid at E10.0 reduces this meningeal neural crest and inhibits parietal ossification, suggesting that intramembranous ossification of this mesodermal bone requires interaction with neural crest-derived meninges, whereas ossification of the neural crest-derived frontal bone is autonomous. These observations provide new perspectives on skull evolution and on human genetic abnormalities of skull growth and ossification.
    MeSH term(s) Animals ; Biological Evolution ; Body Patterning ; Brain/embryology ; Cranial Sutures/embryology ; Genetic Markers ; Meninges/embryology ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Neural Crest/cytology ; Osteogenesis/drug effects ; Parietal Bone/drug effects ; Parietal Bone/embryology ; Proto-Oncogene Proteins/genetics ; Skull/embryology ; Tretinoin/pharmacology ; Wnt Proteins ; Wnt1 Protein ; Zebrafish Proteins
    Chemical Substances Genetic Markers ; Proto-Oncogene Proteins ; Wnt Proteins ; Wnt1 Protein ; Wnt1 protein, mouse ; Zebrafish Proteins ; Tretinoin (5688UTC01R)
    Language English
    Publishing date 2002-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1114-9
    ISSN 1095-564X ; 0012-1606
    ISSN (online) 1095-564X
    ISSN 0012-1606
    DOI 10.1006/dbio.2001.0487
    Database MEDical Literature Analysis and Retrieval System OnLINE

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