scholarly journals Multiple roles for FGF-3 during cranial neural development in the chicken

Development ◽  
1995 ◽  
Vol 121 (5) ◽  
pp. 1399-1410 ◽  
Author(s):  
R. Mahmood ◽  
P. Kiefer ◽  
S. Guthrie ◽  
C. Dickson ◽  
I. Mason
Keyword(s):  
Neural Development ◽  
Primitive Streak ◽  
Neural Plate ◽  
Multiple Roles ◽  
Posterior Half ◽  
Temporal Expression ◽  
Pharyngeal Arches ◽  
Early Organogenesis ◽  
Vertebrate Embryos ◽  
Associated Function

FGF-3 has been implicated in the development of the hindbrain and otocyst in vertebrate embryos. Since the chicken embryo offers a favourable system in which to study the development of these structures, we have isolated and characterised cDNAs for chicken Fgf-3 and determined its pattern of expression in chick embryos from stage 3 (primitive streak) to stage 25 (early organogenesis). Within the developing cranial neural tube, Fgf-3 exhibits dynamic spatial and temporal expression. During extension of the head process, RNA is detected in the midline of the developing neural plate. In neurulating embryos, transcripts are observed initially in rhombomeres 4 and 5 of the hindbrain and later, in rhombomere 6. During hindbrain development, expression is lost from these rhombomeres, but becomes restricted to rhombomere boundaries, providing an intracellular marker which distinguishes a population of cells within boundary regions. Fgf-3 expression is elevated in ventral and medial boundary regions and is greatly reduced in dorsal parts. Studies of regenerating rhombomere boundaries show that Fgf-3 expression is induced in reforming boundaries when even-numbered rhombomere tissue is grafted next to odd, but not when like is juxtaposed to like. Fgf-3 disappears from boundary regions just prior to the loss of the morphological boundaries suggesting a boundary-associated function. Other sites of expression have also been identified. At early stages of development Fgf-3 is expressed in the epiblast and mesendoderm of the primitive streak, in mesoderm lateral to the streak and in Hensen's node. In older embryos transcripts are detected in the endoderm of the pharyngeal pouches, the ectoderm of the second and third pharyngeal arches and the stomodeum. Expression was also detected in the segmental plate and in the posterior half of the three most-recently generated somites.

scholarly journals Visceral endoderm-restricted translation of Otx1 mediates recovery of Otx2 requirements for specification of anterior neural plate and normal gastrulation

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 5091-5104 ◽  
Author(s):  
D. Acampora ◽  
V. Avantaggiato ◽  
F. Tuorto ◽  
P. Briata ◽  
G. Corte ◽  
...  
Keyword(s):  
Transcriptional Control ◽  
Expression Patterns ◽  
Epileptic Seizures ◽  
Primitive Streak ◽  
Neural Plate ◽  
Visceral Endoderm ◽  
Temporal Expression ◽  
Biochemical Activity ◽  
The Difference ◽  
Anterior Neural Plate

Otx1 and Otx2, two murine homologs of the Drosophila orthodenticle (otd) gene, contribute to brain morphogenesis. In particular Otx1 null mice are viable and show spontaneous epileptic seizures and abnormalities affecting the dorsal telencephalic cortex. Otx2 null mice die early in development and fail in specification of the rostral neuroectoderm and proper gastrulation. In order to determine whether Otx1(−/−)and Otx2(−/−) highly divergent phenotypes reflect differences in temporal expression or biochemical activity of OTX1 and OTX2 proteins, the Otx2-coding sequence was replaced by a human Otx1 full-coding cDNA. Homozygous mutant embryos recovered anterior neural plate and proper gastrulation but failed to maintain forebrain-midbrain identities, displaying a headless phenotype from 9 days post coitum (d.p.c.) onwards. Unexpectedly, in spite of the RNA distribution in both visceral endoderm (VE) and epiblast, the hOTX1 protein was synthesized only in the VE. This VE-restricted translation was sufficient to recover Otx2 requirements for specification of the anterior neural plate and proper organization of the primitive streak, thus providing evidence that the difference between Otx1 and Otx2 null mice phenotypes originates from their divergent expression patterns. Moreover, our data lead us to hypothesize that the differential post-transcriptional control existing between VE and epiblast cells may potentially contribute to fundamental regulatory mechanisms required for head specification.

scholarly journals Initiation of Murine Embryonic Erythropoiesis: A Spatial Analysis

Blood ◽  
1997 ◽  
Vol 89 (4) ◽  
pp. 1154-1164 ◽  
Author(s):  
Louise Silver ◽  
James Palis
Keyword(s):  
Expression Patterns ◽  
Erythroid Differentiation ◽  
Primitive Streak ◽  
Neural Plate ◽  
Temporal Expression ◽  
Targeted Disruption ◽  
Mesoderm Cell ◽  
Temporal And Spatial ◽  
Extraembryonic Mesoderm

Abstract Hematopoiesis in the mouse conceptus begins in the visceral yolk (VYS), with primitive erythroblasts first evident in blood islands at the headfold stage (E8.0). VYS erythropoiesis is decreased or abrogated by targeted disruption of the hematopoietic transcription factors tal-1, rbtn2, GATA-1, and GATA-2. To better understand the potential roles of these genes, and to trace the initial temporal and spatial development of mammalian embryonic hematopoiesis, we examined their expression patterns, and that of βH1-globin, in normal mouse conceptuses by means of in situ hybridization. Attention was focused on the 36-hour period from mid-primitive streak to early somite stages (E7.25 to E8.5), when the conceptus undergoes rapid morphologic changes with formation of the yolk sac and blood islands. Each of these genes was expressed in extraembryonic mesoderm, from which blood islands are derived. This VYS expression occurred in a defined temporal sequence: tal-1 and rbtn2 transcripts were detected earlier than the others, followed by GATA-2 and GATA-1, and then by βH1-globin. Transcripts for all of these genes were present in VYS mesoderm cell masses at the neural plate stage (E7.5), indicating commitment of these cells to the erythroid lineage before the appearance of morphologically recognizable erythroblasts. By early somite stages (E8.5), GATA-2 mRNA expression is downregulated in VYS blood islands as terminal primitive erythroid differentiation proceeds. We conclude that primitive mammalian erythropoiesis arises during gastrulation through the ordered temporal expression of tal-1, rbtn2, GATA2, and GATA-1 in a subset of extraembryonic mesoderm cells. During the stages analyzed, tal-1 and rbtn2 expression was also present in posterior embryonic mesoderm, while GATA-1 and GATA-2 expression was evident in extraembryonic tissues of ectodermal origin.

scholarly journals Transcriptional response of Hoxb genes to retinoid signalling is regionally restricted along the neural tube rostrocaudal axis

2017 ◽  
Vol 4 (4) ◽  
pp. 160913 ◽  
Author(s):  
Nicoletta Carucci ◽  
Emanuele Cacci ◽  
Paola S. Nisi ◽  
Valerio Licursi ◽  
Yu-Lee Paul ◽  
...  
Keyword(s):  
Neural Tube ◽  
Neural Development ◽  
Transcriptional Response ◽  
Neural Tissue ◽  
Positional Information ◽  
Multiple Roles ◽  
Chromatin Activation ◽  
Neural Stem Progenitor Cells ◽  
Rostrocaudal Axis

During vertebrate neural development, positional information is largely specified by extracellular morphogens. Their distribution, however, is very dynamic due to the multiple roles played by the same signals in the developing and adult neural tissue. This suggests that neural progenitors are able to modify their competence to respond to morphogen signalling and autonomously maintain positional identities after their initial specification. In this work, we take advantage of in vitro culture systems of mouse neural stem/progenitor cells (NSPCs) to show that NSPCs isolated from rostral or caudal regions of the mouse neural tube are differentially responsive to retinoic acid (RA), a pivotal morphogen for the specification of posterior neural fates. Hoxb genes are among the best known RA direct targets in the neural tissue, yet we found that RA could promote their transcription only in caudal but not in rostral NSPCs. Correlating with these effects, key RA-responsive regulatory regions in the Hoxb cluster displayed opposite enrichment of activating or repressing histone marks in rostral and caudal NSPCs. Finally, RA was able to strengthen Hoxb chromatin activation in caudal NSPCs, but was ineffective on the repressed Hoxb chromatin of rostral NSPCs. These results suggest that the response of NSPCs to morphogen signalling across the rostrocaudal axis of the neural tube may be gated by the epigenetic configuration of target patterning genes, allowing long-term maintenance of intrinsic positional values in spite of continuously changing extrinsic signals.

scholarly journals Experiments on the Development of the Head of the Chick Embryo

1936 ◽  
Vol 13 (2) ◽  
pp. 219-236
Author(s):  
C. H. WADDINGTON ◽  
A. COHEN
Keyword(s):  
Thin Sheet ◽  
Neural Tissue ◽  
Primitive Streak ◽  
Neural Plate ◽  
Head Region ◽  
Process Stage ◽  
Optic Vesicles ◽  
Lens Formation ◽  
Embryonic Ectoderm

1. Experiments were made on the development of the head of chicken embryos cultivated in vitro. 2. Defects in the presumptive head region of primitive streak embryos are regulated completely if the wound fills up before the histogenesis of neural tissue begins in the head-process stage. Different methods by which the hole is filled are described. 3. No repair occurs in the head-process and head-fold stages, and in this period two masses of neural tissue cannot heal together. 4. Median defects, even if repaired as regards neural tissue, cause a failure of the ventral closure of the foregut. The lateral evaginations of the gut develop typically in atypical situations. The headfold may break through and join up with the endoderm in such a way that the gut acquires an anterior opening. 5. The paired heart rudiments may develop separately. The separate vesicles begin to contract at a time appropriate to the development of the embryo as a whole. The two hearts are mirror images, the left one having the normal curvature, but the embryos do not survive long enough for the hearts to acquire a very definite shape. 6. The forebrain has a considerable capacity for repair in the early somite stages (five to twenty-five somites). One-half of the forebrain can remodel itself into a complete forebrain. In some cases the neural plate and epidermis grow together over the wound, in others the epidermis and mesenchyme make the first covering, leaving a space along the inside of which the neural tissue grows. The neural tissue may become a very thin sheet. 7. The repaired forebrain may induce the formation of a nasal placode from the non-presumptive nasal epidermis which covers the wound. 8. If the optic vesicle is entirely removed, a new one is not formed, but parts of the vesicle can regulate to complete eye-cups, either when still attached to the forebrain or after being isolated in the extra-embryonic regions of another embryo. 9. Injured optic vesicles induce lenses from the non-presumptive epidermis which grows over the wound. Transplanted optic neural tissue from embryos of about five somites induces the formation of lentoids from extra-embryonic ectoderm, but only in a small proportion of cases. 10. The presumptive lens epidermis can produce a slight thickening even when contact with the optic cup is prevented. 11. The significance of periods of minimum regulatory power for the concept of determination is discussed. 12. The data concerning lens formation are discussed in terms of the field concept.

XBF-2 is a transcriptional repressor that converts ectoderm into neural tissue

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 5019-5031 ◽  
Author(s):  
F.V. Mariani ◽  
R.M. Harland
Keyword(s):  
Dna Binding ◽  
Neural Development ◽  
Ectopic Expression ◽  
Transcriptional Repressor ◽  
Neural Plate ◽  
Binding Domain ◽  
Expression Cloning ◽  
Dna Binding Domain ◽  
Neural Fate ◽  
Striking Contrast

We have identified Xenopus Brain Factor 2 (XBF-2) as a potent neuralizing activity in an expression cloning screen. In ectodermal explants, XBF-2 converts cells from an epidermal to a neural fate. Such explants contain neurons with distinct axonal profiles and express both anterior and posterior central nervous system (CNS) markers. In striking contrast to X-ngnR-1a or X-NeuroD, ectopic expression of XBF-2 in Xenopus embryos results in an expansion of the neural plate to the ventral midline. The enlarged neural plate consists predominantly of undifferentiated neurons. XBF-2 lies downstream of the BMP antagonists noggin, cerberus, and gremlin since ectodermal explants expressing these molecules exhibit strong expression of XBF-2. While XBF-2 does not upregulate the expression of secreted neural inducers, it downregulates the transcription of BMP-4, an epidermal inducer. We show that XBF-2 acts as a transcriptional repressor and that its effects can be phenocopied with either the engrailed or hairy repressor domain fused to the XBF-2 DNA-binding domain. A fusion of the DNA-binding domain to the activator domain of VP16 blocks the effects of XBF-2 and prevents neural plate development in the embryo. This provides evidence that a transcriptional repressor can affect both regional neural development and neurogenesis in vertebrates.

Developmental expression of the alpha receptor for platelet-derived growth factor, which is deleted in the embryonic lethal Patch mutation

Development ◽  
1992 ◽  
Vol 115 (1) ◽  
pp. 289-303 ◽  
Author(s):  
A. Orr-Urtreger ◽  
M.T. Bedford ◽  
M.S. Do ◽  
L. Eisenbach ◽  
P. Lonai
Keyword(s):  
Primitive Streak ◽  
Yolk Sac ◽  
Developmental Expression ◽  
Wild Type ◽  
Neural Tubes ◽  
Pdgfra Gene ◽  
Branchial Arches ◽  
Early Organogenesis ◽  
Visceral Yolk Sac ◽  
Parietal Endoderm

The alpha receptor of PDGF (Pdgfra) is expressed in primitive endoderm and mesoderm derivatives throughout embryogenesis. In the early primitive streak stage the gene is transcribed in the visceral and parietal endoderm. Later it is expressed in the presomitic mesoderm, yolk sac and amnion. During somitogenesis its transcription localizes to the heart and the somites. Subsequently, it is transcribed in the dermatome, the sclerotome, the developing limb and in various mesenchymal tissues of visceral organs. Its wild-type expression pattern correlates well with the phenotype of homozygous mutant Patch (Ph) embryos, where the Pdgfra gene is deleted. The Ph phenotype is first detectable at the primitive streak stage with convoluted and hypertrophic visceral yolk sac, deformed neural plate and disorganized or missing mesoderm. Most Ph/Ph embryos die before the 11th day of gestation. Those that survive till early organogenesis are very small, have hypertrophic yolk sacs, small and undifferentiated somites, convoluted neural tubes, large heart and pericardium, rudimentary limb buds and branchial arches. Our observations together suggest that the alpha PDGF receptor may be required for the normal development of visceral endoderm and mesoderm derivatives.

The spatial and temporal dynamics of Sax1 (CHox3) homeobox gene expression in the chick's spinal cord

Development ◽  
1994 ◽  
Vol 120 (7) ◽  
pp. 1817-1828 ◽  
Author(s):  
P. Spann ◽  
M. Ginsburg ◽  
Z. Rangini ◽  
A. Fainsod ◽  
H. Eyal-Giladi ◽  
...  
Keyword(s):  
Temporal Dynamics ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Neural Plate ◽  
Transverse Plane ◽  
Posterior Border ◽  
Anterior Border ◽  
Spatial And Temporal Dynamics ◽  
Specific Localization

Sax1 (previously CHox3) is a chicken homeobox gene belonging to the same homeobox gene family as the Drosophila NK1 and the honeybee HHO genes. Sax1 transcripts are present from stage 2 H&H until at least 5 days of embryonic development. However, specific localization of Sax1 transcripts could not be detected by in situ hybridization prior to stage 8-, when Sax1 transcripts are specifically localized in the neural plate, posterior to the hindbrain. From stages 8- to 15 H&H, Sax1 continues to be expressed only in the spinal part of the neural plate. The anterior border of Sax1 expression was found to be always in the transverse plane separating the youngest somite from the yet unsegmented mesodermal plate and to regress with similar dynamics to that of the segregation of the somites from the mesodermal plate. The posterior border of Sax1 expression coincides with the posterior end of the neural plate. In order to study a possible regulation of Sax1 expression by its neighboring tissues, several embryonic manipulation experiments were performed. These manipulations included: removal of somites, mesodermal plate or notochord and transplantation of a young ectopic notochord in the vicinity of the neural plate or transplantation of neural plate sections into the extraembryonic area. The results of these experiments revealed that the induction of the neural plate by the mesoderm has already occurred in full primitive streak embryos, after which Sax1 is autonomously regulated within the spinal part of the neural plate.

Ectodermal patterning in the avian embryo: epidermis versus neural plate

Development ◽  
1999 ◽  
Vol 126 (1) ◽  
pp. 63-73 ◽  
Author(s):  
E. Pera ◽  
S. Stein ◽  
M. Kessel
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Plate Boundary ◽  
Homeobox Gene ◽  
Primitive Streak ◽  
Neural Plate ◽  
Avian Embryo ◽  
Neural Fate ◽  
Early Stages ◽  
Two Factors

Ectodermal patterning of the chick embryo begins in the uterus and continues during gastrulation, when cells with a neural fate become restricted to the neural plate around the primitive streak, and cells fated to become the epidermis to the periphery. The prospective epidermis at early stages is characterized by the expression of the homeobox gene DLX5, which remains an epidermal marker during gastrulation and neurulation. Later, some DLX5-expressing cells become internalized into the ventral forebrain and the neural crest at the hindbrain level. We studied the mechanism of ectodermal patterning by transplantation of Hensen's nodes and prechordal plates. The DLX5 marker indicates that not only a neural plate, but also a surrounding epidermis is induced in such operations. Similar effects can be obtained with neural plate grafts. These experiments demonstrate that the induction of a DLX5-positive epidermis is triggered by the midline, and the effect is transferred via the neural plate to the periphery. By repeated extirpations of the endoderm we suppressed the formation of an endoderm/mesoderm layer under the epiblast. This led to the generation of epidermis, and to the inhibition of neuroepithelium in the naked ectoderm. This suggests a signal necessary for neural, but inhibitory for epidermal development, normally coming from the lower layers. Finally, we demonstrate that BMP4, as well as BMP2, is capable of inducing epidermal fate by distorting the epidermis-neural plate boundary. This, however, does not happen independently within the neural plate or outside the normal DLX5 domain. In the area opaca, the co-transplantation of a BMP4 bead with a node graft leads to the induction of DLX5, thus indicating the cooperation of two factors. We conclude that ectodermal patterning is achieved by signalling both from the midline and from the periphery, within the upper but also from the lower layers.

scholarly journals Neural Induction, Neural Fate Stabilization, and Neural Stem Cells

2002 ◽  
Vol 2 ◽  
pp. 1147-1166 ◽  
Author(s):  
Sally A. Moody ◽  
Hyun-Soo Je
Keyword(s):  
Stem Cells ◽  
Embryonic Stem Cells ◽  
Neural Stem Cells ◽  
Neural Development ◽  
Current Knowledge ◽  
Embryonic Stem ◽  
Neural Induction ◽  
Neural Plate ◽  
Natural Rate ◽  
Neural Fate

The promise of stem cell therapy is expected to greatly benefit the treatment of neurodegenerative diseases. An underlying biological reason for the progressive functional losses associated with these diseases is the extremely low natural rate of self-repair in the nervous system. Although the mature CNS harbors a limited number of self-renewing stem cells, these make a significant contribution to only a few areas of brain. Therefore, it is particularly important to understand how to manipulate embryonic stem cells and adult neural stem cells so their descendants can repopulate and functionally repair damaged brain regions. A large knowledge base has been gathered about the normal processes of neural development. The time has come for this information to be applied to the problems of obtaining sufficient, neurally committed stem cells for clinical use. In this article we review the process of neural induction, by which the embryonic ectodermal cells are directed to form the neural plate, and the process of neural�fate stabilization, by which neural plate cells expand in number and consolidate their neural fate. We will present the current knowledge of the transcription factors and signaling molecules that are known to be involved in these processes. We will discuss how these factors may be relevant to manipulating embryonic stem cells to express a neural fate and to produce large numbers of neurally committed, yet undifferentiated, stem cells for transplantation therapies.

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