Neural induction and regionalisation in the chick embryo

Development ◽  
1992 ◽  
Vol 114 (3) ◽  
pp. 729-741 ◽  
Author(s):  
K.G. Storey ◽  
J.M. Crossley ◽  
E.M. De Robertis ◽  
W.E. Norris ◽  
C.D. Stern
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Molecular Markers ◽  
Chick Embryo ◽  
Normal Development ◽  
Neural Induction ◽  
Stage 4 ◽  
Embryo Chick ◽  
Host Embryo ◽  
Embryonic Region

Induction and regionalisation of the chick nervous system were investigated by transplanting Hensen's node into the extra-embryonic region (area opaca margin) of a host embryo. Chick/quail chimaeras were used to determine the contributions of host and donor tissue to the supernumerary axis, and three molecular markers, Engrailed, neurofilaments (antibody 3A10) and XlHbox1/Hox3.3 were used to aid the identification of particular regions of the ectopic axis. We find that the age of the node determines the regions of the nervous system that form: young nodes (stages 2–4) induced both anterior and posterior nervous system, while older nodes (stages 5–6) have reduced inducing ability and generate only posterior nervous system. By varying the age of the host embryo, we show that the competence of the epiblast to respond to neural induction declines after stage 4. We conclude that during normal development, the initial steps of neural induction take place before stage 4 and that anteroposterior regionalisation of the nervous system may be a later process, perhaps associated with the differentiating notochord. We also speculate that the mechanisms responsible for induction of head CNS differ from those that generate the spinal cord: the trunk CNS could arise by homeogenetic induction by anterior CNS or by elongation of neural primordia that are induced very early.

The L5 epitope: an early marker for neural induction in the chick embryo and its involvement in inductive interactions

Development ◽  
1991 ◽  
Vol 112 (4) ◽  
pp. 959-970 ◽  
Author(s):  
C. Roberts ◽  
N. Platt ◽  
A. Streit ◽  
M. Schachner ◽  
C.D. Stern
Keyword(s):  
Nervous System ◽  
Chick Embryo ◽  
Neural Induction ◽  
Primitive Streak ◽  
Hybridoma Cells ◽  
Minor Components ◽  
Lower Molecular Mass ◽  
Host Embryo ◽  
Donor Embryo ◽  
Developing Nervous System

The pattern of expression of the carbohydrate epitope L5 was studied during early development of the chick neuroepithelium. Immunoreactivity first appears during gastrulation, at mid-primitive streak stage, and persists until at least 3.5 days of development. The epitope is expressed on all the components of the developing nervous system, both central and peripheral. In immunoblots, the antibody recognises a major component of about Mr 500,000 and several more minor components of lower molecular mass. If a Hensen's node from a donor embryo is transplanted into the area opaca of a host embryo, L5 immunoreactivity appears in the epiblast surrounding the graft. If hybridoma cells secreting the antibody are grafted together with Hensen's node into a host chick embryo, the induction of a supernumerary nervous system is inhibited. We suggest that the L5 epitope is an early and general marker for neural induction and that it may be involved directly in inductive interactions.

Neurodevelopment

2012 ◽  
pp. 156-160
Author(s):  
Karl Zilles
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Cerebral Cortex ◽  
Genetic Factors ◽  
Neural Induction ◽  
The Central Nervous System

This chapter discusses neural induction, organogenesis of the central nervous system, histogenesis of the spinal cord, histogenesis of the brainstem and cerebellum, histogenesis of the cerebral cortex, hemispheric shape and the formation of gyri, and genetic factors during development.

The prechordal region lacks neural inducing ability, but can confer anterior character to more posterior neuroepithelium

Development ◽  
1997 ◽  
Vol 124 (15) ◽  
pp. 2983-2996 ◽  
Author(s):  
A.C. Foley ◽  
K.G. Storey ◽  
C.D. Stern
Keyword(s):  
Nervous System ◽  
Molecular Markers ◽  
Primitive Streak ◽  
Neural Fate ◽  
Spemann's Organizer ◽  
Stage 4

The avian equivalent of Spemann's organizer, Hensen's node, begins to lose its ability to induce a nervous system from area opaca epiblast cells at stage 4+, immediately after the full primitive streak stage. From this stage, the node is no longer able to induce regions of the nervous system anterior to the hindbrain. Stage 4+ is marked by the emergence from the node of a group of cells, the prechordal mesendoderm. Here we have investigated whether the prechordal region possesses the lost functions of the organizer, using quail-chick chimaeras to distinguish graft- and host-derived cells, together with several region-specific molecular markers. We find that the prechordal region does not have neural inducing ability, as it is unable to divert extraembryonic epiblast cells to a neural fate. However, it can confer more anterior character to prospective hindbrain cells of the host, making them acquire expression of the forebrain markers tailless and Otx-2. It can also rescue the expression of Krox-20 and Otx-2 from nervous system induced by an older (stage 5) node in extraembryonic epiblast. We show that these properties reflect a true change of fate of cells rather than recruitment from other regions. The competence of neuroectoderm to respond to anteriorizing signals declines by stages 7–9, but both posteriorizing signals and the ability of neuroectoderm to respond to them persist after this stage.

scholarly journals DEPRESSION OF ANAEROBIC GLYCOLYSIS OF EMBRYONIC TISSUE BY WESTERN STRAIN OF EQUINE ENCEPHALOMYELITIS VIRUS. PREVENTION OF THIS EFFECT BY SPECIFIC IMMUNE SERUM

1944 ◽  
Vol 79 (2) ◽  
pp. 129-135 ◽  
Author(s):  
Joseph Victor ◽  
C. H. Huang
Keyword(s):  
Skeletal Muscle ◽  
Spinal Cord ◽  
Chick Embryo ◽  
Immune Serum ◽  
Embryonic Tissue ◽  
Anaerobic Glycolysis ◽  
Embryonic Tissues ◽  
Encephalomyelitis Virus ◽  
Embryo Chick ◽  
Brain And Spinal Cord

Studies were made on the effect of mixing the Western strain of equine encephalomyelitis virus (W.E.E.) and embryonic tissue on the rate of anaerobic glycolysis of the tissue. Whole chick embryo, chick embryo from which brain and spinal cord had been removed, and embryonic skeletal muscle were employed. 1. W.E.E. virus depressed the rate of anaerobic glycolysis of embryonic tissues within 2 days after its addition to the tissue. The decrease in anaerobic glycolysis varied from 17 to 82 per cent and was apparent 2 to 4 days after the addition of the virus. No significant effect of the virus was observed 4 hours and 6 days after mixing it with the tissue. 2. Anti-W.E.E. immune serum prevented the inhibiting action of W.E.E. virus on the anaerobic glycolysis of embryonic skeletal muscle.

Preventing the loss of competence for neural induction: HGF/SF, L5 and Sox-2

Development ◽  
1997 ◽  
Vol 124 (6) ◽  
pp. 1191-1202 ◽  
Author(s):  
A. Streit ◽  
S. Sockanathan ◽  
L. Perez ◽  
M. Rex ◽  
P.J. Scotting ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Transcription Factor ◽  
Molecular Level ◽  
Neural Induction ◽  
Signalling Molecules ◽  
Stage 4 ◽  
Related Transcription Factor ◽  
Neural Marker ◽  
First Time ◽  
Extracellular Signalling

The response to neural induction depends on the presence of inducing signals and on the state of competence of the responding tissue. The epiblast of the chick embryo loses its ability to respond to neural induction by the organizer (Hensen's node) between stages 4 and 4+. We find that the pattern of expression of the L5(220) antigen closely mirrors the changes in competence of the epiblast in time and in space. For the first time, we describe an experiment that can extend the period of neural competence: when L5(220) expression is maintained beyond its normal time by implanting HGF/SF secreting cells, the competence to respond to Hensen's node grafts is retained. The host epiblast forms a non-regionalized neural tube, which expresses the pan-neural marker SOX-2 (a Sry-related transcription factor) but not any region-specific markers for the forebrain, hindbrain or spinal cord. Although HGF/SF secreting cells can mimic signals from Hensen's node that maintain L5 expression, they cannot rescue the ability of the node to induce anterior structures (which is normally lost after stage 4). The ectoderm may acquire stable neural characteristics during neural induction by going through a hierarchy of states: competence, neuralization and regionalization. Our findings allow us to start to define these different states at a molecular level, and show that the competence to respond to neural induction is not entirely autonomous to the responding cells, but can be regulated by extracellular signalling molecules.

Axial mesendoderm refines rostrocaudal pattern in the chick nervous system

Development ◽  
1999 ◽  
Vol 126 (13) ◽  
pp. 2921-2934 ◽  
Author(s):  
A.M. Rowan ◽  
C.D. Stern ◽  
K.G. Storey
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Molecular Markers ◽  
Regional Differences ◽  
Normal Development ◽  
De Novo ◽  
Neural Plate ◽  
Large Panel ◽  
The Central Nervous System

There has long been controversy concerning the role of the axial mesoderm in the induction and rostrocaudal patterning of the vertebrate nervous system. Here we investigate the neural inducing and regionalising properties of defined rostrocaudal regions of head process/prospective notochord in the chick embryo by juxtaposing these tissues with extraembryonic epiblast or neural plate explants. We localise neural inducing signals to the emerging head process and using a large panel of region-specific neural markers, show that different rostrocaudal levels of the head process derived from headfold stage embryos can induce discrete regions of the central nervous system. However, we also find that rostral and caudal head process do not induce expression of any of these molecular markers in explants of the neural plate. During normal development the head process emerges beneath previously induced neural plate, which we show has already acquired some rostrocaudal character. Our findings therefore indicate that discrete regions of axial mesendoderm at headfold stages are not normally responsible for the establishment of rostrocaudal pattern in the neural plate. Strikingly however, we do find that caudal head process inhibits expression of rostral genes in neural plate explants. These findings indicate that despite the ability to induce specific rostrocaudal regions of the CNS de novo, signals provided by the discrete regions of axial mesendoderm do not appear to establish regional differences, but rather refine the rostrocaudal character of overlying neuroepithelium.

β-Mannosidosis: Myelin and oligodendrocyte lesions in brain and spinal cord

1984 ◽  
Vol 42 ◽  
pp. 694-695
Author(s):  
Kathryn L. Lovell ◽  
Margaret Z. Jones
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Genetic Disorder ◽  
Neurological Deficits ◽  
Axonal Spheroids ◽  
South Wales ◽  
Pendular Nystagmus ◽  
Myelin Deficits ◽  
Recessive Defect ◽  
Brain And Spinal Cord

Caprine β-mannosidosis, an autosomal recessive defect of glycoprotein catabolism, is associated with a deficiency of tissue and plasma -mannosidase and with tissue accumulation and urinary excretion of oligosaccharides, including the trisaccharide Man(β1-4)GlcNAc(βl-4)GlcNAc and the disaccharide Man(β1-4)GlcNAc. This genetic disorder is evident at birth, with severe neurological deficits including a marked intention tremor, pendular nystagmus, ataxia and inability to stand. Major pathological characteristics described in Nubian goats in Michigan and in Anglo-Nubian goats in New South Wales include widespread cytoplasmic vacuolation in the nervous system and viscera, axonal spheroids, and severe myelin paucity in the brain but not spinal cord or peripheral nerves. Light microscopic examination revealed marked regional variation in the severity of central nervous system myelin deficits, with some brain areas showing nearly complete absence of myelin and other regions characterized by the presence of 25-50% of the control number of myelin sheaths.

Alterations in the number of motoneurons containing immunoreactive calcitonin gene-related peptide(CGRP)& choline acetyltransferase(ChAT) in the cervical spinal cord of the wobbler mouse during the development of the motoneuron disease

1995 ◽  
Vol 53 ◽  
pp. 970-971
Author(s):  
L. Vacca-Galloway ◽  
Y.Q. Zhang ◽  
P. Bose ◽  
S.H. Zhang
Keyword(s):  
Spinal Cord ◽  
Early Stage ◽  
Cervical Spinal Cord ◽  
Wild Type Mouse ◽  
Reflex Response ◽  
Mouse Strains ◽  
Behavioral Tests ◽  
Wobbler Mouse ◽  
Stage 4 ◽  
Stage 1

The Wobbler mouse (wr) has been studied as a model for inherited human motoneuron diseases (MNDs). Using behavioral tests for forelimb power, walking, climbing, and the “clasp-like reflex” response, the progress of the MND can be categorized into early (Stage 1, age 21 days) and late (Stage 4, age 3 months) stages. Age-and sex-matched normal phenotype littermates (NFR/wr) were used as controls (Stage 0), as well as mice from two related wild-type mouse strains: NFR/N and a C57BI/6N. Using behavioral tests, we also detected pre-symptomatic Wobblers at postnatal ages 7 and 14 days. The mice were anesthetized and perfusion-fixed for immunocytochemical (ICC) of CGRP and ChAT in the spinal cord (C3 to C5).Using computerized morphomety (Vidas, Zeiss), the numbers of IR-CGRP labelled motoneurons were significantly lower in 14 day old Wobbler specimens compared with the controls (Fig. 1). The same trend was observed at 21 days (Stage 1) and 3 months (Stage 4). The IR-CGRP-containing motoneurons in the Wobbler specimens declined progressively with age.

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