Endocytic Protein Defects in the Neural Crest Cell Lineage and Its Pathway Are Associated with Congenital Heart Defects
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Induction and Specification of Cranial Placodes ⁎ Gerhard Schlosser
Developmental Biology 294 (2006) 303–351 www.elsevier.com/locate/ydbio Review Induction and specification of cranial placodes ⁎ Gerhard Schlosser Brain Research Institute, AG Roth, University of Bremen, FB2, PO Box 330440, 28334 Bremen, Germany Received for publication 6 October 2005; revised 22 December 2005; accepted 23 December 2005 Available online 3 May 2006 Abstract Cranial placodes are specialized regions of the ectoderm, which give rise to various sensory ganglia and contribute to the pituitary gland and sensory organs of the vertebrate head. They include the adenohypophyseal, olfactory, lens, trigeminal, and profundal placodes, a series of epibranchial placodes, an otic placode, and a series of lateral line placodes. After a long period of neglect, recent years have seen a resurgence of interest in placode induction and specification. There is increasing evidence that all placodes despite their different developmental fates originate from a common panplacodal primordium around the neural plate. This common primordium is defined by the expression of transcription factors of the Six1/2, Six4/5, and Eya families, which later continue to be expressed in all placodes and appear to promote generic placodal properties such as proliferation, the capacity for morphogenetic movements, and neuronal differentiation. A large number of other transcription factors are expressed in subdomains of the panplacodal primordium and appear to contribute to the specification of particular subsets of placodes. This review first provides a brief overview of different cranial placodes and then synthesizes evidence for the common origin of all placodes from a panplacodal primordium. The role of various transcription factors for the development of the different placodes is addressed next, and it is discussed how individual placodes may be specified and compartmentalized within the panplacodal primordium. -
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. -
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. -
Sox9 Is Required for Invagination of the Otic Placode in Mice ⁎ Francisco Barrionuevo A, , Angela Naumann B, Stefan Bagheri-Fam A,1, Volker Speth C, Makoto M
Available online at www.sciencedirect.com Developmental Biology 317 (2008) 213–224 www.elsevier.com/developmentalbiology Sox9 is required for invagination of the otic placode in mice ⁎ Francisco Barrionuevo a, , Angela Naumann b, Stefan Bagheri-Fam a,1, Volker Speth c, Makoto M. Taketo d, Gerd Scherer a, Annette Neubüser b a Institute of Human Genetics and Anthropology, University of Freiburg, Breisacherstr. 33, D-79106 Freiburg, Germany b Developmental Biology, Institute of Biology 1, University of Freiburg, Hauptstrasse 1, D-79104 Freiburg, Germany c Cell Biology, Institute of Biology II, University of Freiburg, Schänzlestrasse 1, D-79104 Freiburg, Germany d Department of Pharmacology, Graduate School of Medicine, Kyoto University, Yoshida-Konoé-cho, Sakyo-ku, Kyoto 606-8501, Japan Received for publication 20 December 2007; revised 7 February 2008; accepted 8 February 2008 Available online 21 February 2008 Abstract The HMG-domain-containing transcription factor Sox9 is an important regulator of chondrogenesis, testis formation and development of several other organs. Sox9 is expressed in the otic placodes, the primordia of the inner ear, and studies in Xenopus have provided evidence that Sox9 is required for otic specification. Here we report novel and different functions of Sox9 during mouse inner ear development. We show that in mice with a Foxg1Cre-mediated conditional inactivation of Sox9 in the otic ectoderm, otic placodes form and express markers of otic specification. However, mutant placodes do not attach to the neural tube, fail to invaginate, and subsequently degenerate by apoptosis, resulting in a complete loss of otic structures. Transmission-electron microscopic analysis suggests that cell–cell contacts in the Sox9 mutant placodes are abnormal, although E-cadherin, N-cadherin, and beta-catenin protein expression are unchanged. -
Migratory Patterns and Developmental Potential of Trunk Neural Crest Cells in the Axolotl Embryo
DEVELOPMENTAL DYNAMICS 236:389–403, 2007 RESEARCH ARTICLE Migratory Patterns and Developmental Potential of Trunk Neural Crest Cells in the Axolotl Embryo Hans-Henning Epperlein,1* Mark A.J. Selleck,2 Daniel Meulemans,3 Levan Mchedlishvili,4 Robert Cerny,5 Lidia Sobkow,4 and Marianne Bronner-Fraser3 Using cell markers and grafting, we examined the timing of migration and developmental potential of trunk neural crest cells in axolotl. No obvious differences in pathway choice were noted for DiI-labeling at different lateral or medial positions of the trunk neural folds in neurulae, which contributed not only to neural crest but also to Rohon-Beard neurons. Labeling wild-type dorsal trunks at pre- and early-migratory stages revealed that individual neural crest cells migrate away from the neural tube along two main routes: first, dorsolaterally between the epidermis and somites and, later, ventromedially between the somites and neural tube/notochord. Dorsolaterally migrating crest primarily forms pigment cells, with those from anterior (but not mid or posterior) trunk neural folds also contributing glia and neurons to the lateral line. White mutants have impaired dorsolateral but normal ventromedial migration. At late migratory stages, most labeled cells move along the ventromedial pathway or into the dorsal fin. Contrasting with other anamniotes, axolotl has a minor neural crest contribution to the dorsal fin, most of which arises from the dermomyotome. Taken together, the results reveal stereotypic migration and differentiation of neural crest cells in axolotl that differ from other vertebrates in timing of entry onto the dorsolateral pathway and extent of contribution to some derivatives. -
Cell Delamination in the Mesencephalic Neural Fold and Its
© 2013. Published by The Company of Biologists Ltd | Development (2013) 140, 4890-4902 doi:10.1242/dev.094680 RESEARCH ARTICLE Cell delamination in the mesencephalic neural fold and its implication for the origin of ectomesenchyme Raymond Teck Ho Lee1, Hiroki Nagai2, Yukiko Nakaya2, Guojun Sheng2, Paul A. Trainor3,4, James A. Weston5 and Jean Paul Thiery1,6,7,* ABSTRACT dorsal neural fold epithelia (Hörstadius, 1950) suggested that the The neural crest is a transient structure unique to vertebrate embryos neural crest is the source of multipotent stem cells that give rise to that gives rise to multiple lineages along the rostrocaudal axis. In a remarkable diversity of cell types, including pigment cells, neurons cranial regions, neural crest cells are thought to differentiate into and glia of the peripheral and enteric nervous systems. In addition, chondrocytes, osteocytes, pericytes and stromal cells, which are the neural crest was widely considered to be the source of collectively termed ectomesenchyme derivatives, as well as pigment mesenchymal connective tissues that entered the branchial arches to and neuronal derivatives. There is still no consensus as to whether form components of the craniofacial skeleton and connective tissue the neural crest can be classified as a homogenous multipotent of the dorsal fin at the trunk axial levels of fishes and amphibia population of cells. This unresolved controversy has important (Hörstadius, 1950; Le Douarin and Kalcheim, 1999; Raven, 1936). implications for the formation of ectomesenchyme and for Grafting studies in avian embryos (Le Douarin and Teillet, 1974; confirmation of whether the neural fold is compartmentalized into Nakamura and Ayer-le Lievre, 1982) suggested that developmental distinct domains, each with a different repertoire of derivatives. -
And Krox-20 and on Morphological Segmentation in the Hindbrain of Mouse Embryos
The EMBO Journal vol.10 no.10 pp.2985-2995, 1991 Effects of retinoic acid excess on expression of Hox-2.9 and Krox-20 and on morphological segmentation in the hindbrain of mouse embryos G.M.Morriss-Kay, P.Murphy1,2, R.E.Hill1 and in embryos are unknown, but in human embryonal D.R.Davidson' carcinoma cells they include the nine genes of the Hox-2 cluster (Simeone et al., 1990). Department of Human Anatomy, South Parks Road, Oxford OXI 3QX The hindbrain and the neural crest cells derived from it and 'MRC Human Genetics Unit, Western General Hospital, Crewe are of particular interest in relation to the developmental Road, Edinburgh EH4 2XU, UK functions of RA because they are abnormal in rodent 2Present address: Istituto di Istologia ed Embriologia Generale, embryos exposed to a retinoid excess during or shortly before Universita di Roma 'la Sapienza', Via A.Scarpa 14, 00161 Roma, early neurulation stages of development (Morriss, 1972; Italy Morriss and Thorogood, 1978; Webster et al., 1986). Communicated by P.Chambon Human infants exposed to a retinoid excess in utero at early developmental stages likewise show abnormalities of the Mouse embryos were exposed to maternally administered brain and of structures to which cranial neural crest cells RA on day 8.0 or day 73/4 of development, i.e. at or just contribute (Lammer et al., 1985). Retinoid-induced before the differentiation of the cranial neural plate, and abnormalities of hindbrain morphology in rodent embryos before the start of segmentation. On day 9.0, the RA- include shortening of the preotic region in relation to other treated embryos had a shorter preotic hindbrain than the head structures, so that the otocyst lies level with the first controls and clear rhombomeric segmentation was pharyngeal arch instead of the second (Morriss, 1972; absent. -
The Role of Proteoglycans in the Initiation of Neural Tube Closure
The role of proteoglycans in the initiation of neural tube closure Oleksandr Nychyk Thesis submitted to UCL for the degree of Doctor of Philosophy 2017 Developmental Biology of Birth Defects Developmental Biology & Cancer Programme UCL Great Ormond Street Institute of Child Health Declaration of contribution I, Oleksandr Nychyk confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in my thesis. ___________________________________________ Oleksandr Nychyk 2 Abstract Neurulation is the embryonic process that gives rise to the neural tube (NT), the precursor of the brain and spinal cord. Recent work has emphasised the importance of proteoglycans in convergent extension movements and NT closure in lower vertebrates. The current study is focused on the role of proteoglycans in the initiation of NT closure in mammals, termed closure 1. In this project, the initial aim was to characterise the ‘matrisome’, or in vivo extracellular matrix (ECM) composition, during mammalian neurulation. Tissue site of mRNA expression and protein localisation of ECM components, including proteoglycans, were then investigated showing their distinct expression patterns prior to and after the onset of neural tube closure. The expression analysis raised various hypothesis that were subsequently tested, demonstrating that impaired sulfation of ECM proteoglycan chains worsens the phenotype of planar cell polarity (PCP) mutant loop tail (Vangl2Lp) predisposed to neural tube defects. Exposure of Vangl2Lp/+ embryos to chlorate, an inhibitor of glycosaminoglycan sulfation, during ex vivo whole embryo culture prevented NT closure, converting Vangl2Lp/+ to the mutant Vangl2Lp/Lp pathophenotype. The same result was obtained by exposure of Vangl2Lp/+ + embryos to chondroitinase or heparitinase. -
Determination in the Cranial Neural Crest of the Axolotl
Determination in the Cranial Neural Crest of the Axolotl by D. R. NEWTH1 Department of Zoology and Comparative Anatomy, University College London WITH ONE PLATE INTRODUCTION UNCERTAINTY exists on the stage of development at which the cartilagenous component of the cranial neural crest in amphibian embryos becomes com- mitted to its presumptive fate. Earlier results, and particularly those of Raven (1933, 1935) on Triturus and Axolotl, suggested that this determination has occurred by the open medullary plate stage, since pieces of neural fold from the head region could give rise to cartilage after homoplastic transplantation to the trunk. Later this conclusion was challenged by Horstadius & Sellman (1946). In their hands urodele neural fold from the branchial region failed to form cartilage when transplanted to the flank or when substituted for trunk neural fold, unless other tissues (head mesoderm or endoderm) were transplanted with it, or unless the somites of the host in the region of the graft were mechanically damaged at the time of grafting. They conclude that the differentiation of cartilage from cells of the neural fold takes place only after they have been subject to influences from outside themselves—in other words they are not fully determined at this stage. An important, and possibly significant, difference between the experimental procedure of Raven and that of Horstadius & Sellman lies in the age at which their host animals were killed for histological study. Raven's animals were killed after reaching relatively advanced larval stages. The Swedish authors, by con- trast, killed their animals at the beginning of larval life (21 days after operation). -
(MMP-2) in Ectomesenchyme-Derived Tissues of the Patch Mutant Mouse: Regulation of MMP-2 by PDGF and Effects on Mesenchymal Cell Migration
Developmental Biology 212, 255–263 (1999) Article ID dbio.1999.9373, available online at http://www.idealibrary.com on Diminished Matrix Metalloproteinase 2 (MMP-2) in Ectomesenchyme-Derived Tissues of the Patch Mutant Mouse: Regulation of MMP-2 by PDGF and Effects on Mesenchymal Cell Migration James R. Robbins, Paul G. McGuire, Bernhard Wehrle-Haller,* and Sherry L. Rogers1 Department of Cell Biology and Physiology, University of New Mexico School of Medicine, 149 Basic Medical Sciences Building, Albuquerque, New Mexico 87131; and *De´partment de Pathologie, Centre Medical Universitaire, 1 Rue Michel-Servet, CH-1211 Geneva 4, Switzerland Platelet-derived growth factors (PDGF) regulate cell proliferation, survival, morphology, and migration, as well as deposition and turnover of the extracellular matrix. Important roles for the A form of PDGF (PDGF-A) during connective tissue morphogenesis have been highlighted by the murine Patch mutation, which includes a deletion of the a subunit of the PDGF receptor. Homozygous (Ph/Ph) embryos exhibit multiple connective tissue defects including cleft face (involving the first branchial arch and frontonasal processes), incomplete heart septation, and heart valve abnormalities before they die in utero. Analyses of the cell biology underlying the defects in Ph/Ph embryos have revealed a deficit in a matrix metalloproteinase (MMP-2) and one of its activators (MT-MMP) that are likely to be involved in cell migration and tissue remodeling, two processes necessary for normal cardiac and craniofacial development. Morphogenesis of these structures requires infiltration of ectomesenchymal precursors and their subsequent deposition and remodeling of extracellular matrix components. First branchial arch and heart tissue from E10.5 embryos were examined by gelatin zymography and RT-PCR in order to characterize the expression of MMPs in these tissues. -
20. Placodes and Sensory Development
PLACODES AND 20. SENSORY DEVELOPMENT Letty Moss-Salentijn DDS, PhD Dr. Edwin S. Robinson Professor of Dentistry (in Anatomy and Cell Biology) E-mail: [email protected] READING ASSIGNMENT: Larsen 3rd Edition Chapter 12, Part 2. pp.379-389; Part 3. pp.390- 396; Chapter 13, pp.430-432 SUMMARY A series of ectodermal thickenings or placodes develop in the cephalic region at the periphery of the neural plate. Placodes are central to the development of the cranial sensory systems in vertebrates and are among the innovations that appeared in the early evolution of vertebrates. There are placodes for the three organs of special sense: olfactory, optic (lens) and otic placodes, and (epibranchial) placodes that give rise to the distal cells of the sensory ganglia of cranial nerves V, VII, IX and X. Placodes (with the possible exception of the olfactory placodes) form under the influence of surrounding cranial tissues. They do not appear to require the presence of neural crest. The mesoderm in the prechordal plate plays a significant role in the initial development of the placodes for the organs of special sense, while the pharyngeal pouch endoderm plays that role in the development of the epibranchial placodes. The development of the organs of special sense is described briefly. LEARNING OBJECTIVES You should be able to: a. Give a definition of placodes and describe their evolutionary significance. b. Name the different types of placodes, their locations in the developing embryo and their developmental fates. c. Discuss the early development of the placodes and some of the possible factors that feature in their development. -
Migration and Differentiation of Neural Crest and Ventral Neural Tube Cells in Vitro: Implications for in Vitro and in Vivo Studies of the Neural Crest
The Journal of Neuroscience, March 1988, 8(3): 1001-l 01.5 Migration and Differentiation of Neural Crest and Ventral Neural Tube Cells in vitro: Implications for in vitro and in vivo Studies of the Neural Crest J. F. Loring,’ D. L. Barker;,= and C. A. Erickson’ ‘Department of Zoology, University of California, Davis, California 95616, and *Hatfield Marine Sciences Center, Newport, Oregon 97365 During vertebrate development, neural crest cells migrate trunk neural crest cell cultures, a number of classicalneuro- from the dorsal neural tube and give rise to pigment cells transmitters have been reported, including catecholamines(Co- and most peripheral ganglia. To study these complex pro- hen, 1977; Loring et al., 1982;Maxwell et al., 1982) ACh (Kahn cesses it is helpful to make use of in vitro techniques, but et al., 1980; Maxwell et al., 1982) GABA (Maxwell et al., 1982), the transient and morphologically ill-defined nature of neural and 5-HT (Sieber-Blum et al., 1983). In addition, neuroactive crest cells makes it difficult to isolate a pure population of peptides, suchas somatostatin (Maxwell et al., 1984) have been undifferentiated cells. We have used several established reported in neural crest cell culture. techniques to obtain neural crest-containing cultures from In spite of the advantagesof an in vitro approachto analysis quail embryos and have compared their subsequent differ- of neural crest differentiation, it is clear that a fundamental entiation. We confirm earlier reports of neural crest cell dif- problem ariseswhen attempts are made to isolate these cellsin ferentiation in vitro into pigment cells and catecholamine- culture.