The Neuromeric Model of Brain Development/Evolution 12.12.12

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The Neuromeric Model of Brain Development/Evolution 12.12.12 Thursday, December 13, 12 Replication and Segmentation Thursday, December 13, 12 DV patterning of neural tube (the Bauplan) Jessell 2000 Thursday, December 13, 12 DV patterning of neural tube in forebrain (the Bauplan) Puelles and Rubenstein 2003 Thursday, December 13, 12 The Columnar model of JB Johnson and CJ Herrick (First World War and onwards) Anterior Dorsal Anterior Posterior Left Right Ventral Posterior Thursday, December 13, 12 Segmentation Thursday, December 13, 12 Hox genes Thursday, December 13, 12 Loss of function (Antennapaedia) Gain of function (Bithorax) Thursday, December 13, 12 Somites and evolution Richardson et al. 1998 Thursday, December 13, 12 Hox genes Thursday, December 13, 12 Hox genes Thursday, December 13, 12 The Neuromeric model of Von Kuppfer, His and Orr (Pre War) Anterior Dorsal Anterior Posterior Left Right Ventral Posterior Thursday, December 13, 12 Rhombomeres Lumsden and Keynes 1989 Thursday, December 13, 12 Rhombomeres as compartments Lumsden 2004 Thursday, December 13, 12 Rhombomeres and cranial nerves Chick Human Lumsden and Keynes 1989 Thursday, December 13, 12 Hox genes provide a unique code for rhombomere identity while other genes set up boundaries Hauptmann et al. 2002 Thursday, December 13, 12 Knockdown and ectopic expression of hoxb-1 Lumsden 2004 Thursday, December 13, 12 The Neuromeric model with a kink Dorsal Dorsal Anterior Posterior Ventral Ventral Dorsal Dorsal Anterior Posterior Ventral Ventral Flexure Thursday, December 13, 12 Vestigial anatomical designations of the columnar model that can be explained by neuromeric model with a kink Dorsal Epithalamus Dorsal thalamus Anterior Posterior Ventral thalamus Hypothalamus Ventral Thursday, December 13, 12 Original Prosomere model Bulfone et al. 1993 Thursday, December 13, 12 Original Prosomere model Puelles and Rubenstein 1993 Thursday, December 13, 12 Segmental scaffold of primary axon fascicles Figdor and Stern 1993 Thursday, December 13, 12 Lineage restriction Figdor and Stern 1993 Thursday, December 13, 12 Ectopic expression of mesomere homeobox gene Otx-2 rostralizes a rhombomere Hidalgo-Sanchez et al. 2005 Thursday, December 13, 12 New conservative Prosomere model Puelles 2009 Thursday, December 13, 12 Neuromeres are not added throughout vertebrate evolution Scholpp and Lumsden 2010 Thursday, December 13, 12 Organizers and chemical signals Kiecker and Lumsden 2003, 2012 Thursday, December 13, 12 Puelles and Rubenstein 2003 Thursday, December 13, 12 Puelles and Rubinstein 2003 Thursday, December 13, 12.

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The Genetic Basis of Mammalian Neurulation
REVIEWS THE GENETIC BASIS OF MAMMALIAN NEURULATION Andrew J. Copp*, Nicholas D. E. Greene* and Jennifer N. Murdoch‡ More than 80 mutant mouse genes disrupt neurulation and allow an in-depth analysis of the underlying developmental mechanisms. Although many of the genetic mutants have been studied in only rudimentary detail, several molecular pathways can already be identified as crucial for normal neurulation. These include the planar cell-polarity pathway, which is required for the initiation of neural tube closure, and the sonic hedgehog signalling pathway that regulates neural plate bending. Mutant mice also offer an opportunity to unravel the mechanisms by which folic acid prevents neural tube defects, and to develop new therapies for folate-resistant defects. 6 ECTODERM Neurulation is a fundamental event of embryogenesis distinct locations in the brain and spinal cord .By The outer of the three that culminates in the formation of the neural tube, contrast, the mechanisms that underlie the forma- embryonic (germ) layers that which is the precursor of the brain and spinal cord. A tion, elevation and fusion of the neural folds have gives rise to the entire central region of specialized dorsal ECTODERM, the neural plate, remained elusive. nervous system, plus other organs and embryonic develops bilateral neural folds at its junction with sur- An opportunity has now arisen for an incisive analy- structures. face (non-neural) ectoderm. These folds elevate, come sis of neurulation mechanisms using the growing battery into contact (appose) in the midline and fuse to create of genetically targeted and other mutant mouse strains NEURAL CREST the neural tube, which, thereafter, becomes covered by in which NTDs form part of the mutant phenotype7.At A migratory cell population that future epidermal ectoderm.
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Clonal Dispersion During Neural Tube Formation 4097 of Neuromeres
Development 126, 4095-4106 (1999) 4095 Printed in Great Britain © The Company of Biologists Limited 1999 DEV2458 Successive patterns of clonal cell dispersion in relation to neuromeric subdivision in the mouse neuroepithelium Luc Mathis1,*, Johan Sieur1, Octavian Voiculescu2, Patrick Charnay2 and Jean-François Nicolas1,‡ 1Unité de Biologie moléculaire du Développement, Institut Pasteur, 25, rue du Docteur Roux, 75724 Paris Cedex 15, France 2Unité INSERM 368, Ecole Normale Supérieure, 46 rue d’Ulm, 75230 Paris Cedex 05, France *Present address: Beckman Institute (139-74), California Institute of Technology, Pasadena, CA, 91125, USA ‡Author for correspondence (e-mail: [email protected]) Accepted 5 July; published on WWW 23 August 1999 SUMMARY We made use of the laacz procedure of single-cell labelling the AP and DV axis of the neural tube. A similar sequence to visualize clones labelled before neuromere formation, in of AP cell dispersion followed by an arrest of AP cell 12.5-day mouse embryos. This allowed us to deduce two dispersion, a preferential DV cell dispersion and then by a successive phases of cell dispersion in the formation of the coherent neuroepithelial growth, is also observed in the rhombencephalon: an initial anterior-posterior (AP) cell spinal cord and mesencephalon. This demonstrates that a dispersion, followed by an asymmetrical dorsoventral (DV) similar cascade of cell events occurs in these different cell distribution during which AP cell dispersion occurs in domains of the CNS. In the prosencephalon, differences in territories smaller than one rhombomere. We conclude that spatial constraints may explain the variability in the the general arrest of AP cell dispersion precedes the onset orientation of cell clusters.
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And Krox-20 and on Morphological Segmentation in the Hindbrain of Mouse Embryos
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Cephalic Neurulation in the Mouse Embryo Analyzed by SEM and Morphometry
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CENTRÁLNÍ a PERIFERNÍ NERVOVÝ SYSTÉM Mikroskopická Stavba A
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Flexion [Recovered]
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Early Stages of the Brain of Acanthias
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Sonic Hedgehog Signaling Directs Patterned Cell Remodeling During
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Ectoderm: Neurulation, Neural Tube, Neural Crest
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Neural Crest Formation in the Head of the Mouse Embryo As Observed Using a New Histological Technique
J. Embryol. exp. Morph. Vol. 64, pp. 105-120, 1981 \ Q5 Printed in Great Britain © Company of Biologists Limited 1981 Neural crest formation in the head of the mouse embryo as observed using a new histological technique By DAVID H. NICHOLS1 From the Department of Anatomy, School of Medicine, University of Virginia SUMMARY A histological technique is described which results in the differential staining of neural crest cells. This is used to describe the formation and early migration of crest cells in the head of the mouse embryo. The first indications of crest formation are seen in the midbrain/ anterior hindbrain at 3-4 somites where crest cells accumulate in the basal surface of the ectodermal epithelium near the future margin of the neural plate. Shortly thereafter (4-6 somites) these cells disrupt the basal surface of the epithelium and escape as mesenchyme. The apical epithelial cells in this region become the surface ectoderm adjacent to the neural plate. Subsequently, crest is formed from neural plate rather than surface ectoderm. In addition, mesenchyme is formed from presumptive surface ectoderm in a groove in the lateral portion of the fold between the forebrain and the midbrain. By 5-7 somites, crest mesenchyme is formed at all levels of the midbrain, hindbrain, and from the margins of the forebrain adjacent to the optic pits. Because of the bending of the embryonic axis, forebrain crest cells appear to migrate dorsally over the presumptive eye where they are met by ventrally migrating midbrain crest cells. Crest formation continues in the region of the midbrain and hindbrain during, and for an undetermined period after closure of the head folds at between 8 and 16 somites.
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Homocysteine and CSRP-3 Protein in Migrating Neural Crest Cells: a Quantitative and Qualitative Confocal Microscopy Study
University of Northern Iowa UNI ScholarWorks Dissertations and Theses @ UNI Student Work 2016 Homocysteine and CSRP-3 protein in migrating neural crest cells: A quantitative and qualitative confocal microscopy study Allysan R. White University of Northern Iowa Let us know how access to this document benefits ouy Copyright ©2016 Allysan R. White Follow this and additional works at: https://scholarworks.uni.edu/etd Part of the Cell Biology Commons, and the Developmental Biology Commons Recommended Citation White, Allysan R., "Homocysteine and CSRP-3 protein in migrating neural crest cells: A quantitative and qualitative confocal microscopy study" (2016). Dissertations and Theses @ UNI. 338. https://scholarworks.uni.edu/etd/338 This Open Access Thesis is brought to you for free and open access by the Student Work at UNI ScholarWorks. It has been accepted for inclusion in Dissertations and Theses @ UNI by an authorized administrator of UNI ScholarWorks. For more information, please contact [email protected]. Copyright by ALLYSAN WHITE 2016 All Rights Reserved HOMOCYSTEINE AND CSRP-3 PROTEIN IN MIGRATING NEURAL CREST CELLS – A QUANTITATIVE AND QUALITATIVE CONFOCAL MICROSCOPY STUDY An Abstract of a Thesis Submitted in Partial Fulfillment of the Requirements for the Degree Master of Science Allysan R White University of Northern Iowa December 2016 ABSTRACT Congenital heart defects are one of the leading causes of infant death. High maternal blood serum levels of the amino acid homocysteine and the frequency of heart defects are correlated, but the immediate cause is unknown. During early embryonic development, a distinctive population of cells arises dorsally as the neural tube closes, forming the brain and spinal cord.
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