Ectoderm: Neurulation, Neural Tube, Neural Crest
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Notch Signaling Regulates the Differentiation of Neural Crest From
ß 2014. Published by The Company of Biologists Ltd | Journal of Cell Science (2014) 127, 2083–2094 doi:10.1242/jcs.145755 RESEARCH ARTICLE Notch signaling regulates the differentiation of neural crest from human pluripotent stem cells Parinya Noisa1,2, Carina Lund2, Kartiek Kanduri3, Riikka Lund3, Harri La¨hdesma¨ki3, Riitta Lahesmaa3, Karolina Lundin2, Hataiwan Chokechuwattanalert2, Timo Otonkoski4,5, Timo Tuuri5,6,* and Taneli Raivio2,4,*,` ABSTRACT Kokta et al., 2013). Neural crest cells originate from neuroectoderm at the border between the neural plate and the Neural crest cells are specified at the border between the neural epiderm (Meulemans and Bronner-Fraser, 2004), and they are plate and the epiderm. They are capable of differentiating into marked by the expression of genes that are specific for the neural- various somatic cell types, including craniofacial and peripheral plate border, such as DLX5, MSX1, MSX2 and ZIC1. Later, during nerve tissues. Notch signaling plays important roles during the neural-tube folding process, neural crest cells remain within neurogenesis; however, its function during human neural crest the neural folds and subsequently localize inside the dorsal development is poorly understood. Here, we generated self- portion of the neural tube. These premigratory neural crest cells renewing premigratory neural-crest-like cells (pNCCs) from human express specifier genes, such as SNAIL (also known as SNAI1), pluripotent stem cells (hPSCs) and investigated the roles of Notch SLUG (also known as SNAI2), SOX10 and TWIST1 (LaBonne and signaling during neural crest differentiation. pNCCs expressed Bronner-Fraser, 2000; Mancilla and Mayor, 1996). Following the various neural-crest-specifier genes, including SLUG (also known formation of the neural tube, premigratory neural crest cells as SNAI2), SOX10 and TWIST1, and were able to differentiate into undergo an epithelial-to-mesenchymal transition (EMT) and most neural crest derivatives. -
The Migration of Neural Crest Cells and the Growth of Motor Axons Through the Rostral Half of the Chick Somite
/. Embryol. exp. Morph. 90, 437-455 (1985) 437 Printed in Great Britain © The Company of Biologists Limited 1985 The migration of neural crest cells and the growth of motor axons through the rostral half of the chick somite M. RICKMANN, J. W. FAWCETT The Salk Institute and The Clayton Foundation for Research, California division, P.O. Box 85800, San Diego, CA 92138, U.S.A. AND R. J. KEYNES Department of Anatomy, University of Cambridge, Downing St, Cambridge, CB2 3DY, U.K. SUMMARY We have studied the pathway of migration of neural crest cells through the somites of the developing chick embryo, using the monoclonal antibodies NC-1 and HNK-1 to stain them. Crest cells, as they migrate ventrally from the dorsal aspect of the neural tube, pass through the lateral part of the sclerotome, but only through that part of the sclerotome which lies in the rostral half of each somite. This migration pathway is almost identical to the path which pre- sumptive motor axons take when they grow out from the neural tube shortly after the onset of neural crest migration. In order to see whether the ventral root axons are guided along this pathway by neural crest cells, we surgically excised the neural crest from a series of embryos, and examined the pattern of axon outgrowth approximately 24 h later. In somites which contained no neural crest cells, ventral root axons were still found only in the rostral half of the somite, although axonal growth was slightly delayed. These axons were surrounded by sheath cells, which had presumably migrated out of the neural tube, to a point about 50 jan proximal to the growth cones. -
Cardiac Neural Crest Cells in Development and Regeneration Rajani M
© 2020. Published by The Company of Biologists Ltd | Development (2020) 147, dev188706. doi:10.1242/dev.188706 REVIEW The heart of the neural crest: cardiac neural crest cells in development and regeneration Rajani M. George, Gabriel Maldonado-Velez and Anthony B. Firulli* ABSTRACT on recent developments in understanding cNCC biology and discuss Cardiac neural crest cells (cNCCs) are a migratory cell population that publications that report a cNCC contribution to cardiomyocytes and stem from the cranial portion of the neural tube. They undergo epithelial- heart regeneration. to-mesenchymal transition and migrate through the developing embryo to give rise to portions of the outflow tract, the valves and the arteries of The origin, migration and cell fate specification of cNCCs the heart. Recent lineage-tracing experiments in chick and zebrafish cNCCs were first identified in quail-chick chimera and ablation embryos have shown that cNCCs can also give rise to mature experiments as a subpopulation of cells that contribute to the cardiomyocytes. These cNCC-derived cardiomyocytes appear to be developing aorticopulmonary septum (Kirby et al., 1983). cNCCs required for the successful repair and regeneration of injured zebrafish are induced by a network of signaling factors such as BMPs, FGFs, hearts. In addition, recent work examining the response to cardiac NOTCH and WNT in the surrounding ectoderm that initiate injury in the mammalian heart has suggested that cNCC-derived expression of cNCC specification genes (Sauka-Spengler and cardiomyocytes are involved in the repair/regeneration mechanism. Bronner-Fraser, 2008; Scholl and Kirby, 2009). Transcription However, the molecular signature of the adult cardiomyocytes involved factor networks that include Msx1 and Msx2, Dlx3 and Dlx5, and in this repair is unclear. -
Works Neuroembryology
Swarthmore College Works Biology Faculty Works Biology 1-1-2017 Neuroembryology D. Darnell Scott F. Gilbert Swarthmore College, [email protected] Follow this and additional works at: https://works.swarthmore.edu/fac-biology Part of the Biology Commons Let us know how access to these works benefits ouy Recommended Citation D. Darnell and Scott F. Gilbert. (2017). "Neuroembryology". Wiley Interdisciplinary Reviews: Developmental Biology. Volume 6, Issue 1. DOI: 10.1002/wdev.215 https://works.swarthmore.edu/fac-biology/493 This work is brought to you for free by Swarthmore College Libraries' Works. It has been accepted for inclusion in Biology Faculty Works by an authorized administrator of Works. For more information, please contact [email protected]. HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Wiley Interdiscip Manuscript Author Rev Dev Manuscript Author Biol. Author manuscript; available in PMC 2018 January 01. Published in final edited form as: Wiley Interdiscip Rev Dev Biol. 2017 January ; 6(1): . doi:10.1002/wdev.215. Neuroembryology Diana Darnell1 and Scott F. Gilbert2 1University of Arizona College of Medicine 2Swarthmore College and University of Helsinki Abstract How is it that some cells become neurons? And how is it that neurons become organized in the spinal cord and brain to allow us to walk and talk, to see, recall events in our lives, feel pain, keep our balance, and think? The cells that are specified to form the brain and spinal cord are originally located on the outside surface of the embryo. They loop inward to form the neural tube in a process called neurulation. -
Induction of Motor Neurons by Sonic Hedgehog Is Independent of Floor Plate Differentiation Yasuto Tanabe, Henk Roelink and Thomas M
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Induction of motor neurons by Sonic hedgehog is independent of floor plate differentiation Yasuto Tanabe, Henk Roelink and Thomas M. Jessell Howard Hughes Medical Institute, Deptartment of Biochemistry and Molecular Biophysics, Center for Neurobiology and Behavior, Columbia University, 701 West 168th Street, New York, New York 10032, USA. Background: The differentiation of floor plate cells and transfected with Shh induced both floor plate cells and motor neurons in the vertebrate neural tube appears to be motor neurons when grown in contact with neural plate induced by signals from the notochord. The secreted pro- explants, whereas only motor neurons were induced when tein encoded by the Sonic hedgehog (Shh) gene is expressed the explants were grown at a distance from Shh-trans- by axial midline cells and can induce floor plate cells in fected COS cells. Direct transfection of neural plate cells vivo and in vitro. Motor neurons can also be induced in with an Shh-expression construct induced both floor plate vitro by cells that synthesize Sonic hedgehog protein cells and motor neurons, with motor neuron differentia- (Shh). It remains unclear, however, if the motor-neuron- tion occurring prior to, or coincidentally with, floor plate inducing activity of Shh depends on the synthesis of a dis- differentiation. The induction of motor neurons appears, tinct signaling molecule by floor plate cells. To resolve therefore, not to depend on floor plate differentiation. this issue, we have developed an in vitro assay which Conclusions: The induction of motor neurons by uncouples the notochord-mediated induction of motor Shh does not depend on distinct floor-plate-derived neurons from floor plate differentiation, and have used signaling molecules. -
Gastrulation
Embryology of the spine and spinal cord Andrea Rossi, MD Neuroradiology Unit Istituto Giannina Gaslini Hospital Genoa, Italy [email protected] LEARNING OBJECTIVES: LEARNING OBJECTIVES: 1) To understand the basics of spinal 1) To understand the basics of spinal cord development cord development 2) To understand the general rules of the 2) To understand the general rules of the development of the spine development of the spine 3) To understand the peculiar variations 3) To understand the peculiar variations to the normal spine plan that occur at to the normal spine plan that occur at the CVJ the CVJ Summary of week 1 Week 2-3 GASTRULATION "It is not birth, marriage, or death, but gastrulation, which is truly the most important time in your life." Lewis Wolpert (1986) Gastrulation Conversion of the embryonic disk from a bilaminar to a trilaminar arrangement and establishment of the notochord The three primary germ layers are established The basic body plan is established, including the physical construction of the rudimentary primary body axes As a result of the movements of gastrulation, cells are brought into new positions, allowing them to interact with cells that were initially not near them. This paves the way for inductive interactions, which are the hallmark of neurulation and organogenesis Day 16 H E Day 15 Dorsal view of a 0.4 mm embryo BILAMINAR DISK CRANIAL Epiblast faces the amniotic sac node Hypoblast Primitive pit (primitive endoderm) faces the yolk sac Primitive streak CAUDAL Prospective notochordal cells Dias Dias During -
A Case of Junctional Neural Tube Defect Associated with a Lipoma of the Filum Terminale: a New Subtype of Junctional Neural Tube Defect?
CASE REPORT J Neurosurg Pediatr 21:601–605, 2018 A case of junctional neural tube defect associated with a lipoma of the filum terminale: a new subtype of junctional neural tube defect? Simona Mihaela Florea, MD,1 Alice Faure, MD,2 Hervé Brunel, MD,3 Nadine Girard, MD, PhD,3 and Didier Scavarda, MD1 Departments of 1Pediatric Neurosurgery, 2Pediatric Surgery, and 3Neuroradiology, Hôpital Timone Enfants, Marseille, France The embryological development of the central nervous system takes place during the neurulation process, which in- cludes primary and secondary neurulation. A new form of dysraphism, named junctional neural tube defect (JNTD), was recently reported, with only 4 cases described in the literature. The authors report a fifth case of JNTD. This 5-year-old boy, who had been operated on during his 1st month of life for a uretero-rectal fistula, was referred for evaluation of possible spinal dysraphism. He had urinary incontinence, clubfeet, and a history of delayed walking ability. MRI showed a spinal cord divided in two, with an upper segment ending at the T-11 level and a lower segment at the L5–S1 level, with a thickened filum terminale. The JNTDs represent a recently classified dysraphism caused by an error during junctional neurulation. The authors suggest that their patient should be included in this category as the fifth case reported in the literature and note that this would be the first reported case of JNTD in association with a lipomatous filum terminale. https://thejns.org/doi/abs/10.3171/2018.1.PEDS17492 KEYWORDS junctional neurulation; junctional neural tube defect; spina bifida; dysraphism; spine; congenital HE central nervous system and vertebrae are formed or lipomas of the filum terminale.16 When there are altera- during the neurulation process that occurs early in tions present in both the primary and secondary neurula- the embryonic life and is responsible for the trans- tion we can find mixed dysraphisms that present with ele- Tformation of the flat neural plate into the neural tube (NT). -
Oligodendrocytes in Development, Myelin Generation and Beyond
cells Review Oligodendrocytes in Development, Myelin Generation and Beyond Sarah Kuhn y, Laura Gritti y, Daniel Crooks and Yvonne Dombrowski * Wellcome-Wolfson Institute for Experimental Medicine, Queen’s University Belfast, Belfast BT9 7BL, UK; [email protected] (S.K.); [email protected] (L.G.); [email protected] (D.C.) * Correspondence: [email protected]; Tel.: +0044-28-9097-6127 These authors contributed equally. y Received: 15 October 2019; Accepted: 7 November 2019; Published: 12 November 2019 Abstract: Oligodendrocytes are the myelinating cells of the central nervous system (CNS) that are generated from oligodendrocyte progenitor cells (OPC). OPC are distributed throughout the CNS and represent a pool of migratory and proliferative adult progenitor cells that can differentiate into oligodendrocytes. The central function of oligodendrocytes is to generate myelin, which is an extended membrane from the cell that wraps tightly around axons. Due to this energy consuming process and the associated high metabolic turnover oligodendrocytes are vulnerable to cytotoxic and excitotoxic factors. Oligodendrocyte pathology is therefore evident in a range of disorders including multiple sclerosis, schizophrenia and Alzheimer’s disease. Deceased oligodendrocytes can be replenished from the adult OPC pool and lost myelin can be regenerated during remyelination, which can prevent axonal degeneration and can restore function. Cell population studies have recently identified novel immunomodulatory functions of oligodendrocytes, the implications of which, e.g., for diseases with primary oligodendrocyte pathology, are not yet clear. Here, we review the journey of oligodendrocytes from the embryonic stage to their role in homeostasis and their fate in disease. We will also discuss the most common models used to study oligodendrocytes and describe newly discovered functions of oligodendrocytes. -
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. -
Sonic Hedgehog Induces the Lateral Floor Plate
Development 129, 4785-4796 (2002) 4785 Printed in Great Britain © The Company of Biologists Limited 2002 DEV2912 Dual origin of the floor plate in the avian embryo Jean-Baptiste Charrier, Françoise Lapointe, Nicole M. Le Douarin and Marie-Aimée Teillet* Institut d’Embryologie Cellulaire et Moléculaire, CNRS and Collège de France, UMR 7128, 49bis Avenue de la Belle Gabrielle, 94736 Nogent-sur-Marne Cedex, France *Author for correspondence (e-mail: [email protected]) Accepted 30 July 2002 SUMMARY Molecular analysis carried out on quail-chick chimeras, in development, one can experimentally obtain a complete which quail Hensen’s node was substituted for its chick floor plate in the neural epithelium by the inductive action counterpart at the five- to six-somite stage (ss), showed that of either a notochord or a MFP. The competence of the the floor plate of the avian neural tube is composed of neuroepithelium to respond to notochord or MFP signals is distinct areas: (1) a median one (medial floor plate or MFP) restricted to a short time window, as only the posterior-most derived from Hensen’s node and characterised by the same region of the neural plate of embryos younger than 15 ss is gene expression pattern as the node cells (i.e. expression of able to differentiate a complete floor plate comprising MFP HNF3β and Shh to the exclusion of genes early expressed and LFP. Moreover, MFP differentiation requires between in the neural ectoderm such as CSox1); and (2) lateral 4 and 5 days of exposure to the inducing tissues. -
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. -
Semaphorin3a/Neuropilin-1 Signaling Acts As a Molecular Switch Regulating Neural Crest Migration During Cornea Development
Developmental Biology 336 (2009) 257–265 Contents lists available at ScienceDirect Developmental Biology journal homepage: www.elsevier.com/developmentalbiology Semaphorin3A/neuropilin-1 signaling acts as a molecular switch regulating neural crest migration during cornea development Peter Y. Lwigale a,⁎, Marianne Bronner-Fraser b a Department of Biochemistry and Cell Biology, MS 140, Rice University, P.O. Box 1892, Houston, TX 77251, USA b Division of Biology, 139-74, California Institute of Technology, Pasadena, CA 91125, USA article info abstract Article history: Cranial neural crest cells migrate into the periocular region and later contribute to various ocular tissues Received for publication 2 April 2009 including the cornea, ciliary body and iris. After reaching the eye, they initially pause before migrating over Revised 11 September 2009 the lens to form the cornea. Interestingly, removal of the lens leads to premature invasion and abnormal Accepted 6 October 2009 differentiation of the cornea. In exploring the molecular mechanisms underlying this effect, we find that Available online 13 October 2009 semaphorin3A (Sema3A) is expressed in the lens placode and epithelium continuously throughout eye development. Interestingly, neuropilin-1 (Npn-1) is expressed by periocular neural crest but down- Keywords: Semaphorin3A regulated, in a manner independent of the lens, by the subpopulation that migrates into the eye and gives Neuropilin-1 rise to the cornea endothelium and stroma. In contrast, Npn-1 expressing neural crest cells remain in the Neural crest periocular region and contribute to the anterior uvea and ocular blood vessels. Introduction of a peptide that Cornea inhibits Sema3A/Npn-1 signaling results in premature entry of neural crest cells over the lens that Lens phenocopies lens ablation.