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Craniofacial Morphogenesis (craniofacial + morphogenesi)
Selected AbstractsGeneration and characterization of a novel neural crest marker allele, Inka1-LacZ, reveals a role for Inka1 in mouse neural tube closureDEVELOPMENTAL DYNAMICS, Issue 4 2010Bethany S. Reid Abstract Previous studies identified Inka1 as a gene regulated by AP-2, in the neural crest required for craniofacial morphogenesis in fish and frog. Here, we extend the analysis of Inka1 function and regulation to the mouse by generating a LacZ knock-in allele. Inka1-LacZ allele expression occurs in the cephalic mesenchyme, heart, and paraxial mesoderm prior to E8.5. Subsequently, expression is observed in the migratory neural crest cells and their derivatives. Consistent with expression of Inka1 in tissues of the developing head during neurulation, a low percentage of Inka1,/, mice show exencephaly while the remainder are viable and fertile. Further studies indicate that AP-2, is not required for Inka1 expression in the mouse, and suggest that there is no significant genetic interaction between these two factors during embryogenesis. Together, these data demonstrate that while the expression domain of Inka1 is conserved among vertebrates, its function and regulation are not. Developmental Dynamics 239:1188,1196, 2010. © 2010 Wiley-Liss, Inc. [source] Recent advances in craniofacial morphogenesisDEVELOPMENTAL DYNAMICS, Issue 9 2006Yang Chai Abstract Craniofacial malformations are involved in three fourths of all congenital birth defects in humans, affecting the development of head, face, or neck. Tremendous progress in the study of craniofacial development has been made that places this field at the forefront of biomedical research. A concerted effort among evolutionary and developmental biologists, human geneticists, and tissue engineers has revealed important information on the molecular mechanisms that are crucial for the patterning and formation of craniofacial structures. Here, we highlight recent advances in our understanding of evo,devo as it relates to craniofacial morphogenesis, fate determination of cranial neural crest cells, and specific signaling pathways in regulating tissue,tissue interactions during patterning of craniofacial apparatus and the morphogenesis of tooth, mandible, and palate. Together, these findings will be beneficial for the understanding, treatment, and prevention of human congenital malformations and establish the foundation for craniofacial tissue regeneration. Developmental Dynamics 235:2353,2375, 2006. © 2006 Wiley-Liss, Inc. [source] Facial surface analysis by 3D laser scanning and geometric morphometrics in relation to sexual dimorphism in cerebral,craniofacial morphogenesis and cognitive functionJOURNAL OF ANATOMY, Issue 3 2005Robin J. Hennessy Abstract Over early fetal life the anterior brain, neuroepithelium, neural crest and facial ectoderm constitute a unitary, three-dimensional (3D) developmental process. This intimate embryological relationship between the face and brain means that facial dysmorphogenesis can serve as an accessible and informative index of brain dysmorphogenesis in neurological and psychiatric disorders of early developmental origin. There are three principal challenges in seeking to increase understanding of disorders of early brain dysmorphogenesis through craniofacial dysmorphogenesis: (i) the first, technical, challenge has been to digitize the facial surface in its inherent three-dimensionality; (ii) the second, analytical, challenge has been to develop methodologies for extracting biologically meaningful shape covariance from digitized samples, making statistical comparisons between groups and visualizing in 3D the resultant statistical models on a ,whole face' basis; (iii) the third, biological, challenge is to demonstrate a relationship between facial morphogenesis and brain morphogenesis not only in anatomical,embryological terms but also at the level of brain function. Here we consider each of these challenges in turn and then illustrate the issues by way of our own findings. These use human sexual dimorphism as an exemplar for 3D laser surface scanning of facial shape, analysis using geometric morphometrics and exploration of cognitive correlates of variation in shape of the ,whole face', in the context of studies relating to the early developmental origins of schizophrenia. [source] Prenatal craniofacial morphogenesis: four-dimensional visualization of morphogenetic processesORTHODONTICS & CRANIOFACIAL RESEARCH, Issue 2003RJ Radlanski Structured Abstract Author , Radlanski RJ Objectives , Basic research concerning craniofacial development presently runs along two pathways, namely the molecular and the morphometric. This gap needs to be bridged. Design , Using histological serial sections of human fetuses computer-aided three-dimensional reconstructions were made (Software Analysis, SIS) with special focus given to all anatomical structures of the orofacial region of the growing head. Results , All reconstructions can be viewed from any rotation and they are available for virtual dissection according to anatomical rules. As an example, the prenatal development of the human mandible with the formation of the mental foramen therein is described. Furthermore, the spatial arrangement of bone, cartilage and nerves is presented in three dimensions in different developmental stages. The interaction of tissues with possible morphogenetic interaction is discussed. Conclusions , This work serves as a reference system for prenatal development in comparison with pathological development. [source] Neural and orofacial defects in Folbp1 knockout mice ,BIRTH DEFECTS RESEARCH, Issue 4 2003Louisa S. Tang Abstract BACKGROUND Folic acid is essential for the development of the nervous system and other associated structures. Mice deficient in the folic acid-binding protein one (Folbp1) gene display multiple developmental abnormalities, including neural and craniofacial defects. To better understand potential interactions between Folbp1 gene and selected genes involved in neural and craniofacial morphogenesis, we evaluated the expression patterns of a panel of crucial differentiation markers (Pax-3, En-2, Hox-a1, Shh, Bmp-4, Wnt-1, and Pax-1). METHODS Folbp1 mice were supplemented with low dosages of folinic acid to rescue nullizygotes from dying in utero before gestational day 10. The gene marker analyses were carried out by in situ hybridization. RESULTS In nullizygote embryos with open cranial neural tube defects, the downregulation of Pax-3 and En-2 in the impaired midbrain, along with an observed upregulation of the ventralizing marker Shh in the expanded floor plate, suggested an important regulatory interaction among these three genes. Moreover, the nullizygotes also exhibit craniofacial abnormalities, such as cleft lip and palate. Pax-3 signals in the impaired medial nasal primordia were significantly increased, whereas Pax-1 showed no expression in the undeveloped lateral nasal processes. Although Shh was downregulated, Bmp-4 was strongly expressed in the medial and lateral nasal processes, highlighting the antagonistic activities of these molecules. CONCLUSIONS Impairment of Folbp1 gene function adversely impacts the expression of several critical signaling molecules. Mis-expression of these molecules, perhaps mediated by Shh, may potentially contribute to the observed failure of neural tube closure and the development of craniofacial defects in the mutant mice. Birth Defects Research (Part A) 67:209,218, 2003. © 2003 Wiley-Liss, Inc. [source] | ||||||||||