DOCSLIB.ORG

Significance of the Cranial Neural Crest

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Significance of the Cranial Neural Crest DEVELOPMENTAL DYNAMICS 229:5–13, 2004 REVIEWS–A PEER REVIEWED FORUM Significance of the Cranial Neural Crest Anthony Graham,* Jo Begbie, and Imelda McGonnell The cranial neural crest has long been viewed as being of particular significance. First, it has been held that the cranial neural crest has a morphogenetic role, acting to coordinate the development of the pharyngeal arches. By contrast, the trunk crest seems to play a more subservient role in terms of embryonic patterning. Second, the cranial crest not only generates neurons, glia, and melanocytes, but additionally forms skeletal derivatives (bones, cartilage, and teeth, as well as smooth muscle and connective tissue), and this potential was thought to be a unique feature of the cranial crest. Recently, however, several studies have suggested that the cranial neural crest may not be so influential in terms of patterning, nor so exceptional in the derivatives that it makes. It is now becoming clear that the morphogenesis of the pharyngeal arches is largely driven by the pharyngeal endoderm. Furthermore, it is now apparent that trunk neural crest cells have skeletal potential. However, it has now been demonstrated that a key role for the cranial neural crest streams is to organise the innervation of the hindbrain by the cranial sensory ganglia. Thus, in the past few years, our views of the significance of the cranial neural crest for head development have been altered. Developmental Dynamics 229:5–13, 2004. © 2003 Wiley-Liss, Inc. Key words: neural crest; cranial; endoderm; pharyngeal; sensory Received 22 July 2003; Accepted 22 August 2003 INTRODUCTION cells are subjected to the alternating et al., 1991; Schilling and Kimmel, permissive and inhibitory halves of 1994). The second crest stream, the The established view of the cranial somites, which result in their segmen- hyoid, arises primarily from rhom- neural crest was that it played a piv- tal organisation (Rickmann et al., bomere 4 of the hindbrain and forms otal role in vertebrate head devel- 1985). In the head, the neural crest neurons of the proximal facial gan- opment. It was thought that the cra- nial neural crest carried the cues for cells pour out from the developing glion as well as the constituents of organising the morphogenesis of the brain into a periphery that is devoid the second pharyngeal arch—the head and, uniquely, was the source of somites. Yet, the cranial crest cells hyoid skeleton (Lumsden et al., 1991; of much of the head skeleton. How- do not migrate as a single mass but Schilling and Kimmel, 1994). Finally, ever, it is now becoming apparent are organised into streams, three of the post-otic crest is generated by that we must reassess our views of which can be identified in the devel- rhombomeres 6 and 7 of the hind- the significance of the cranial neural oping head of all vertebrate embry- brain and forms the neurons of the crest, and it is with this reassessment os: trigeminal, hyoid, and post-otic proximal and jugular ganglia, and that this review is concerned. (Fig. 1). The trigeminal crest arises the skeletal components of the pos- from the midbrain and rhom- terior pharyngeal arches (Lumsden bomeres 1 and 2 of the hindbrain et al., 1991; Schilling and Kimmel, MIGRATION OF THE CRANIAL and forms neurons within the trigem- 1994). NEURAL CREST inal ganglion and the components In the trunk, the first migrating neu- The migration of the cranial neural of the orofacial prominences and ral crest cells move ventrally from crest is quite distinct from that of the mandibular arch—the skeleton of the neural tube and migrate trunk. In the trunk, the neural crest the lower and upper jaw (Lumsden through the anterior half sclerotome. MRC Centre for Developmental Neurobiology, New Hunts House, Guys Campus, Kings College London, London, United Kingdom Grant sponsor: The Medical Research Council (UK); Grant sponsor: The Wellcome Trust. *Correspondence to: Anthony Graham, MRC Centre for Developmental Neurobiology, New Hunts House, Guys Campus, Kings College London, London SE1 1UL, UK. E-mail: [email protected] DOI 10.1002/dvdy.10442 © 2003 Wiley-Liss, Inc. 6 GRAHAM ET AL. Fig. 1. Cranial neural crest migrates in three streams. The trigeminal stream (red) emanates from the midbrain (mb), rhombomeres (r) 1 and 2. It migrates into the upper jaw primordia, underneath the eye, and into the first pharyngeal arch (PA1), which forms the lower jaw. The hyoid stream (green), from rhombomere 4, migrates into the second pharyn- geal arch, forming the jaw support. The post-otic stream (purple) emerges from rhombomeres 6 and 7. It populates the caudal pharyn- geal arches, of which there are three in the chick embryo depicted here. Fig. 2. Regionalisation of the pharyn- geal endoderm. Endodermal pharyngeal pouches (pp) sit between the pharyngeal arches and express a range of markers that demonstrate distinct regionalisation. Pax-1 (green) is expressed at the dorsal tip of each pouch. BMP-7 (blue) is ex- pressed in the posterior endodermal mar- gin, while Fgf8 (red) is expressed in the anterior endodermal margin. Shh (yel- low) is expressed at the posterior margin of pouches 2 and 3 only. D, dorsal; V, ventral; P, posterior; A, anterior; mb, mid- brain; r, rhombomere. Fig. 3. Segregation of cranial neural crest establishes correct afferent innervation in the vertebrate head. Whole-mount chick embryo labeled with neurofilament antibody to visualise axonal projections. The trigeminal axons (T) extend toward the hindbrain along the first or trigeminal crest stream (red), entering at rhom- bomere (r) 2. Axons of the geniculate (G) extend along the hyoid crest stream (green), into rhombomere 4. Axons from the petrosal (P) and nodose (N) extend along the post-otic crest stream (pur- ple) into rhombomeres 6 and 7, respectively. Mb, midbrain. CRANIAL NEURAL CREST 7 These cells have a neuronal fate. in the crest primordia of rhombomeres nial neural crest streaming is main- Those that move furthest ventrally 3 and 5, which in turn acts to sponsor tained in other species where focal form the sympathetic ganglia, while the apoptotic elimination of these cell death in rhombomeres 3 and 5 is the remainder cease migration in cells (Graham et al., 1994). In vitro ap- not observed, such as in zebrafish the anterior sclerotome and form plication of Bmp-4 can also promote (Schilling and Kimmel, 1994) and Xe- the dorsal root ganglia. The later mi- crest depletion of rhombomeres 2 nopus embryos (Hensey and Gautier, grating neural crest cells, however, and 6, which correlates with the find- 1998). move dorsolaterally between the ing that much of the hindbrain neural Other work has shown that there dermamyotome and the overlying crest expresses the necessary recep- are additional mechanisms that ectoderm, and these cells will form tors and intracellular effectors to re- could contribute to the streaming of the melanocytes (Weston and But- spond to this factor (Farlie et al., 1999; the neural crest. Several studies ler, 1966; Serbedzija et al., 1990; Smith and Graham, 2001). Bmp-4 will seem to suggest that there are inhib- Erickson et al., 1992). In the head, not induce, however, cell death in itory influences emanating from there is also a correlation between rhombomere 4 neural crest, which rhombomeres 3 and 5, which restrict the timing of crest migration and the corresponds with the finding that the movement of cells across these fates the crest cells follow, but it is these crest cells express the Bmp-4 an- segments. For example, if the neural significantly different. Here, the early tagonist Noggin in addition to the crest primordium of rhombomere 4 is migratory cells populate the pharyn- Bmp receptors and intracellular trans- grafted dorsally in rhombomere 3, geal arches and facial prominences, ducers (Smith and Graham, 2001). even though many neural crest cells and these groups will generate ecto- Thus, the neural crest cell death is lo- are now produced they are de- mesenchymal derivatives: bone, car- calised to rhombomeres 3 and 5 both flected anteriorly and posteriorly tilage, and connective tissue, while by restricting the expression of the (Niederlander and Lumsden, 1996). the later migrating cells stay closer to Bmp-4 ligand to these segments as a This effect could be due to the ex- the developing central nervous sys- result of an inductive interaction from pression in both rhombomeres 3 and tem and generate neurons and glia the flanking segments and through 5ofSema3A, a molecule which is of the cranial ganglia (Baker et al., the expression of Noggin in the neural known to inhibit neural crest migra- 1997). crest cells of rhombomere 4, which tion (Eickholt et al., 1999). Similarly, it are juxtaposed to sites of Bmp-4 ex- has been suggested that the mes- SEGREGATION OF THE CRANIAL pression. enchyme opposite these two seg- Studies in other species have sug- ments is inhibitory to neural crest mi- CREST STREAMS gested that the establishment of the gration (Farlie et al., 1999) and that The segregation of the cranial crest cranial neural crest streams may be this finding is due to the function of is evident as soon as they are gen- somewhat different to that observed ErbB4 in the hindbrain (Golding et erated by, and emerge from, the in chick. In mammalian embryos, cra- al., 2000). These studies help explain neural tube, and it is events within nial neural crest migration com- why the few crest cells generated by the developing hindbrain that are mences before neural tube closure rhombomeres 3 and 5 do not move responsible for establishing this seg- and occurs over a protracted period laterally from these rhombomeres regation. Studies in chick have of time (Morriss-Kay and Tucket, 1991).
Load more

Recommended publications
  • And Late-Migrating Cranial Neural Crest Cell Populations Have Equivalent Developmental Potential in Vivo
    Development 124, 3077-3087 (1997) 3077 Printed in Great Britain © The Company of Biologists Limited 1997 DEV3724 Early- and late-migrating cranial neural crest cell populations have equivalent developmental potential in vivo Clare V. H. Baker1,2,*, Marianne Bronner-Fraser1, Nicole M. Le Douarin2 and Marie-Aimée Teillet2 1Division of Biology, Beckman Institute 139-74, California Institute of Technology, Pasadena, California 91125, USA 2Institut d’Embryologie cellulaire et moléculaire du CNRS et du Collège de France, 49bis avenue de la Belle Gabrielle, 94736 Nogent-sur-Marne Cedex, France *Author for correspondence currently at address1 SUMMARY We present the first in vivo study of the long-term fate and heterochronically for the late-migrating population, it no potential of early-migrating and late-migrating mesen- longer contributes to the jaw skeleton and only forms cephalic neural crest cell populations, by performing dorsal derivatives. When the late-migrating population is isochronic and heterochronic quail-to-chick grafts. Both grafted into a late-stage host whose neural crest had previ- early- and late-migrating populations form melanocytes, ously been ablated, it migrates ventrally into the jaws. neurons, glia, cartilage and bone in isochronic, isotopic Thus, the dorsal fate restriction of the late-migrating mes- chimeras, showing that neither population is lineage- encephalic neural crest cell population in normal develop- restricted. The early-migrating population distributes both ment is due to the presence of earlier-migrating neural dorsally and ventrally during normal development, while crest cells, rather than to any change in the environment or the late-migrating population is confined dorsally and to any intrinsic difference in migratory ability or potential forms much less cartilage and bone.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Pluripotency Factors Regulate Definitive Endoderm Specification Through Eomesodermin
    Downloaded from genesdev.cshlp.org on September 23, 2021 - Published by Cold Spring Harbor Laboratory Press Pluripotency factors regulate definitive endoderm specification through eomesodermin Adrian Kee Keong Teo,1,2 Sebastian J. Arnold,3 Matthew W.B. Trotter,1 Stephanie Brown,1 Lay Teng Ang,1 Zhenzhi Chng,1,2 Elizabeth J. Robertson,4 N. Ray Dunn,2,5 and Ludovic Vallier1,5,6 1Laboratory for Regenerative Medicine, University of Cambridge, Cambridge CB2 0SZ, United Kingdom; 2Institute of Medical Biology, A*STAR (Agency for Science, Technology, and Research), Singapore 138648; 3Renal Department, Centre for Clinical Research, University Medical Centre, 79106 Freiburg, Germany; 4Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, United Kingdom Understanding the molecular mechanisms controlling early cell fate decisions in mammals is a major objective toward the development of robust methods for the differentiation of human pluripotent stem cells into clinically relevant cell types. Here, we used human embryonic stem cells and mouse epiblast stem cells to study specification of definitive endoderm in vitro. Using a combination of whole-genome expression and chromatin immunoprecipitation (ChIP) deep sequencing (ChIP-seq) analyses, we established an hierarchy of transcription factors regulating endoderm specification. Importantly, the pluripotency factors NANOG, OCT4, and SOX2 have an essential function in this network by actively directing differentiation. Indeed, these transcription factors control the expression of EOMESODERMIN (EOMES), which marks the onset of endoderm specification. In turn, EOMES interacts with SMAD2/3 to initiate the transcriptional network governing endoderm formation. Together, these results provide for the first time a comprehensive molecular model connecting the transition from pluripotency to endoderm specification during mammalian development.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Late Effects of Retinoic Acid on Neural Crest and Aspects of Rhombomere Identity
    Development 122, 783-793 (1996) 783 Printed in Great Britain © The Company of Biologists Limited 1996 DEV2020 Late effects of retinoic acid on neural crest and aspects of rhombomere identity Emily Gale1, Victoria Prince2, Andrew Lumsden3, Jon Clarke4, Nigel Holder1 and Malcolm Maden1 1Developmental Biology Research Centre, The Randall Institute, King’s College London, 26-29 Drury Lane, London WC2B 5RL, UK 2Department of Molecular Biology, Princeton University, Washington Road, Princeton, NJ 08544, USA 3MRC Brain Development Programme, Division of Anatomy and Cell Biology, UMDS, Guy’s Hospital, London SE1 9RT, UK 4Department of Anatomy and Developmental Biology, University College, Windeyer Building, Cleveland St., London W1P 6DB, UK SUMMARY We exposed st.10 chicks to retinoic acid (RA), both ment of the facial ganglion in addition to a mis-direction of globally, and locally to individual rhombomeres, to look at the extensions of its distal axons and a dramatic decrease its role in specification of various aspects of hindbrain in the number of contralateral vestibuloacoustic neurons derived morphology. Previous studies have looked at RA normally seen in r4. Only this r4-specific neuronal type is exposure at earlier stages, during axial specification. Stage affected in r4; the motor neuron projections seem normal 10 is the time of morphological segmentation of the in experimental animals. The specificity of this result, hindbrain and is just prior to neural crest migration. combined with the loss of Hoxb-1 expression in r4 and the Rhombomere 4 localised RA injections result in specific work by Krumlauf and co-workers showing gain of con- alterations of pathways some crest cells that normally tralateral neurons co-localised with ectopic Hoxb-1 migrate to sites of differentiation of neurogenic derivatives.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • The Physical Mechanisms of Drosophila Gastrulation: Mesoderm and Endoderm Invagination
    | FLYBOOK DEVELOPMENT AND GROWTH The Physical Mechanisms of Drosophila Gastrulation: Mesoderm and Endoderm Invagination Adam C. Martin1 Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142 ORCID ID: 0000-0001-8060-2607 (A.C.M.) ABSTRACT A critical juncture in early development is the partitioning of cells that will adopt different fates into three germ layers: the ectoderm, the mesoderm, and the endoderm. This step is achieved through the internalization of specified cells from the outermost surface layer, through a process called gastrulation. In Drosophila, gastrulation is achieved through cell shape changes (i.e., apical constriction) that change tissue curvature and lead to the folding of a surface epithelium. Folding of embryonic tissue results in mesoderm and endoderm invagination, not as individual cells, but as collective tissue units. The tractability of Drosophila as a model system is best exemplified by how much we know about Drosophila gastrulation, from the signals that pattern the embryo to the molecular components that generate force, and how these components are organized to promote cell and tissue shape changes. For mesoderm invagination, graded signaling by the morphogen, Spätzle, sets up a gradient in transcriptional activity that leads to the expression of a secreted ligand (Folded gastrulation) and a transmembrane protein (T48). Together with the GPCR Mist, which is expressed in the mesoderm, and the GPCR Smog, which is expressed uniformly, these signals activate heterotrimeric G-protein and small Rho-family G-protein signaling to promote apical contractility and changes in cell and tissue shape. A notable feature of this signaling pathway is its intricate organization in both space and time.
    [Show full text]
  • 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.
    [Show full text]