Expression of an engrailed-related protein is induced in the anterior neural ectoderm of early Xenopus embryos

Development ◽  
1989 ◽  
Vol 106 (3) ◽  
pp. 611-617 ◽  
Author(s):  
A.H. Brivanlou ◽  
R.M. Harland
Keyword(s):  
Nuclear Protein ◽  
Neural Plate ◽  
Brain Cells ◽  
Related Protein ◽  
Anterior Portion ◽  
Head Mesoderm ◽  
C Terminus ◽  
Licl Treatment ◽  
Neural Ectoderm ◽  
Xenopus Laevis Embryos

We have used a monoclonal antibody directed against the C-terminus of the Drosophila invected homeodomain to detect a nuclear protein in brain cells of Xenopus laevis embryos. We refer to this antigen as the Xenopus EN protein. The EN protein is localized at midneurula stage to a band of cells in the anterior portion of the neural plate, on each side of the neural groove. Later in development, the expression coincides with the boundary of the midbrain and hindbrain, and persists at least to the swimming tadpole stage. These properties make the EN protein an excellent molecular marker for anterior neural structures. In embryos where inductive interactions between mesodermal and ectodermal tissues have been perturbed, the expression of the EN protein is altered; in embryos that have been anterodorsalized by LiCl treatment, the region that expresses the EN protein is expanded, but still well organized. In ventralized UV-irradiated embryos, the absence of the protein is correlated with the absence of anterior neural structures. In extreme exogastrulae, where the contacts between head mesoderm and prospective neurectoderm are lost, the EN protein is not expressed.

Functional association of retinoic acid and hedgehog signaling in Xenopus primary neurogenesis

Development ◽  
1999 ◽  
Vol 126 (19) ◽  
pp. 4257-4265 ◽  
Author(s):  
P.G. Franco ◽  
A.R. Paganelli ◽  
S.L. Lopez ◽  
A.E. Carrasco
Keyword(s):  
Retinoic Acid ◽  
Sonic Hedgehog ◽  
Hedgehog Signaling ◽  
Inhibitory Effect ◽  
Neural Plate ◽  
Neural Ectoderm ◽  
Differentiation And Proliferation ◽  
Primary Neurogenesis ◽  
Xenopus Laevis Embryos

Previous work has shown that the posteriorising agent retinoic acid can accelerate anterior neuronal differentiation in Xenopus laevis embryos (Papalopulu, N. and Kintner, C. (1996) Development 122, 3409–3418). To elucidate the role of retinoic acid in the primary neurogenesis cascade, we investigated whether retinoic acid treatment of whole embryos could change the spatial expression of a set of genes known to be involved in neurogenesis. We show that retinoic acid expands the N-tubulin, X-ngnr-1, X-MyT1, X-Δ-1 and Gli3 domains and inhibits the expression of Zic2 and sonic hedgehog in the neural ectoderm, whereas a retinoid antagonist produces opposite changes. In contrast, sonic and banded hedgehog overexpression reduced the N-tubulin stripes, enlarged the neural plate at the expense of the neural crest, downregulated Gli3 and upregulated Zic2. Thus, retinoic acid and hedgehog signaling have opposite effects on the prepattern genes Gli3 and Zic2 and on other genes acting downstream in the neurogenesis cascade. In addition, retinoic acid cannot rescue the inhibitory effect of Notch(ICD), Zic2 or sonic hedgehog on primary neurogenesis. Our results suggest that retinoic acid acts very early, upstream of sonic hedgehog, and we propose a model for regulation of differentiation and proliferation in the neural plate, showing that retinoic acid might be activating primary neurogenesis by repressing sonic hedgehog expression.

Is there a ventral neural ridge in chick embryos? Implications for the origin of adenohypophyseal and other APUD cells

Development ◽  
1980 ◽  
Vol 57 (1) ◽  
pp. 71-78
Author(s):  
N. B. Levy ◽  
Ann Andrew ◽  
B. B. Rawdon ◽  
Beverley Kramer
Keyword(s):  
Neural Crest ◽  
Endocrine Cells ◽  
Ventral Surface ◽  
Neural Plate ◽  
Chick Embryos ◽  
Serial Sections ◽  
Apud Cells ◽  
Surface Ectoderm ◽  
Neural Ectoderm ◽  
Thickened Surface

Two- to ten-somite chick embryos were studied in order to ascertain whether, as has been proposed, there exists a ‘ventral neural ridge’ which gives rise to the hypophyseal (Rathke's) pouch. Serial sections and stereo-microscopy were used. The neural ridges arch around the rostral end of the embryo onto the ventral surface of the head, but no evidence was found for their extension to form a ‘ventral neural ridge’ reaching the stomodaeum: in fact a considerable expanse of non-thickened surface ectoderm was seen to separate the ventral portions of the neural ridges from the stomodaeum. The thickening of neural ectoderm which does appear on the ventral surface of the head results from apposition and fusion of the opposite neural ridges flanking the neural plate and thus the tip of the anterior neuropore - the classically accepted mode of closure of the neuropore. These findings are in accord with the generally accepted concept of the origin of thehypophyseal pouch rather than with its derivation from a ‘ventral neural ridge’. No sign of neural crest formation was encountered ventrally; this observation excludes the possibility that endocrine cells of the APUD series could originate from neural crest in this region.

scholarly journals Origins of the avian neural crest: the role of neural plate-epidermal interactions

Development ◽  
1995 ◽  
Vol 121 (2) ◽  
pp. 525-538 ◽  
Author(s):  
M.A. Selleck ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cell ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Neural Tube Closure ◽  
Whole Embryo Culture ◽  
Early Stages ◽  
Tissue Interactions ◽  
Neural Ectoderm

We have investigated the lineage and tissue interactions that result in avian neural crest cell formation from the ectoderm. Presumptive neural plate was grafted adjacent to non-neural ectoderm in whole embryo culture to examine the role of tissue interactions in ontogeny of the neural crest. Our results show that juxtaposition of non-neural ectoderm and presumptive neural plate induces the formation of neural crest cells. Quail/chick recombinations demonstrate that both the prospective neural plate and the prospective epidermis can contribute to the neural crest. When similar neural plate/epidermal confrontations are performed in tissue culture to look at the formation of neural crest derivatives, juxtaposition of epidermis with either early (stages 4–5) or later (stages 6–10) neural plate results in the generation of both melanocytes and sympathoadrenal cells. Interestingly, neural plates isolated from early stages form no neural crest cells, whereas those isolated later give rise to melanocytes but not crest-derived sympathoadrenal cells. Single cell lineage analysis was performed to determine the time at which the neural crest lineage diverges from the epidermal lineage and to elucidate the timing of neural plate/epidermis interactions during normal development. Our results from stage 8 to 10+ embryos show that the neural plate/neural crest lineage segregates from the epidermis around the time of neural tube closure, suggesting that neural induction is still underway at open neural plate stages.

scholarly journals The C terminus of the nuclear protein NuMA: Phylogenetic distribution and structure

2009 ◽  
Vol 13 (10) ◽  
pp. 2573-2577 ◽  
Author(s):  
Patricia C. Abad ◽  
I. Saira Mian ◽  
Cedric Plachot ◽  
Aniysha Nelpurackal ◽  
Carol Bator-Kelly ◽  
...  
Keyword(s):  
Nuclear Protein ◽  
Phylogenetic Distribution ◽  
C Terminus

Distinct roles for Fgf, Wnt and retinoic acid in posteriorizing the neural ectoderm

Development ◽  
2002 ◽  
Vol 129 (18) ◽  
pp. 4335-4346 ◽  
Author(s):  
Tetsuhiro Kudoh ◽  
Stephen W. Wilson ◽  
Igor B. Dawid
Keyword(s):  
Retinoic Acid ◽  
Neural Plate ◽  
Neural Patterning ◽  
Knock Down ◽  
Complementary Pattern ◽  
Neural Ectoderm ◽  
Morpholino Oligonucleotides ◽  
And Function

Early neural patterning in vertebrates involves signals that inhibit anterior (A) and promote posterior (P) positional values within the nascent neural plate. In this study, we have investigated the contributions of, and interactions between, retinoic acid (RA), Fgf and Wnt signals in the promotion of posterior fates in the ectoderm. We analyze expression and function of cyp26/P450RAI, a gene that encodes retinoic acid 4-hydroxylase, as a tool for investigating these events. Cyp26 is first expressed in the presumptive anterior neural ectoderm and the blastoderm margin at the late blastula. When the posterior neural gene hoxb1b is expressed during gastrulation, it shows a strikingly complementary pattern to cyp26. Using these two genes, as well as otx2 and meis3 as anterior and posterior markers, we show that Fgf and Wnt signals suppress expression of anterior genes, including cyp26. Overexpression of cyp26 suppresses posterior genes, suggesting that the anterior expression of cyp26 is important for restricting the expression of posterior genes. Consistent with this, knock-down of cyp26 by morpholino oligonucleotides leads to the anterior expansion of posterior genes. We further show that Fgf- and Wnt-dependent activation of posterior genes is mediated by RA, whereas suppression of anterior genes does not depend on RA signaling. Fgf and Wnt signals suppress cyp26 expression, while Cyp26 suppresses the RA signal. Thus, cyp26 has an important role in linking the Fgf, Wnt and RA signals to regulate AP patterning of the neural ectoderm in the late blastula to gastrula embryo in zebrafish.

Characterization and real-time imaging of the FTLD-related protein aggregation induced by amyloidogenic peptides

2015 ◽  
Vol 51 (41) ◽  
pp. 8652-8655 ◽  
Author(s):  
Ruei-Yu He ◽  
Yi-Chen Huang ◽  
Chao-Wei Chiang ◽  
Yu-Ju Tsai ◽  
Ting-Juan Ye ◽  
...  
Keyword(s):  
Protein Aggregation ◽  
Real Time ◽  
Live Cells ◽  
Related Protein ◽  
Amyloid Fibers ◽  
Real Time Imaging ◽  
C Terminus ◽  
Amyloidogenic Peptides

Q/N- and G-rich polypeptides from the TDP-43 C-terminus formed amyloid fibers in vitro and induced the aggregation of the transfected TDP-43-EGFP in live cells.

scholarly journals Effects of Shh and Noggin on neural crest formation demonstrate that BMP is required in the neural tube but not ectoderm

Development ◽  
1998 ◽  
Vol 125 (24) ◽  
pp. 4919-4930 ◽  
Author(s):  
M.A. Selleck ◽  
M.I. Garcia-Castro ◽  
K.B. Artinger ◽  
M. Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Sonic Hedgehog ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Bmp Signaling ◽  
Neural Tube Closure ◽  
Dorsal Neural Tube ◽  
Neural Ectoderm ◽  
Tube Closure

To define the timing of neural crest formation, we challenged the fate of presumptive neural crest cells by grafting notochords, Sonic Hedgehog- (Shh) or Noggin-secreting cells at different stages of neurulation in chick embryos. Notochords or Shh-secreting cells are able to prevent neural crest formation at open neural plate levels, as assayed by DiI-labeling and expression of the transcription factor, Slug, suggesting that neural crest cells are not committed to their fate at this time. In contrast, the BMP signaling antagonist, Noggin, does not repress neural crest formation at the open neural plate stage, but does so if injected into the lumen of the closing neural tube. The period of Noggin sensitivity corresponds to the time when BMPs are expressed in the dorsal neural tube but are down-regulated in the non-neural ectoderm. To confirm the timing of neural crest formation, Shh or Noggin were added to neural folds at defined times in culture. Shh inhibits neural crest production at early stages (0-5 hours in culture), whereas Noggin exerts an effect on neural crest production only later (5-10 hours in culture). Our results suggest three phases of neurulation that relate to neural crest formation: (1) an initial BMP-independent phase that can be prevented by Shh-mediated signals from the notochord; (2) an intermediate BMP-dependent phase around the time of neural tube closure, when BMP-4 is expressed in the dorsal neural tube; and (3) a later pre-migratory phase which is refractory to exogenous Shh and Noggin.

scholarly journals A heterodimer of HEB and an E12-related protein interacts with the CD4 enhancer and regulates its activity in T-cell lines.

1993 ◽  
Vol 13 (9) ◽  
pp. 5620-5628 ◽  
Author(s):  
S Sawada ◽  
D R Littman
Keyword(s):  
T Cell ◽  
Protein Binding ◽  
Cell Lines ◽  
Nuclear Protein ◽  
Lymphoid Cells ◽  
Related Protein ◽  
Enhancer Activity ◽  
Nuclear Extracts ◽  
E Box ◽  
T Cell Lines

A T-lymphocyte-specific enhancer located 13 kb upstream of the murine CD4 gene was recently shown to be required for the developmentally regulated expression of CD4. We have previously identified three nuclear protein binding sites in this enhancer; one of these sites, CD4-3, is essential for expression and contains two E-box core motifs (CANNTG) adjacent to each other in the sequence TAACAGGTGTCAGCTGGT. In electrophoretic mobility shift assays using the CD4-3 oligonucleotide as a probe, three nuclear protein complexes, termed CD4-3A, -B, and -C, were detected with nuclear extracts from T-cell lines. CD4-3A, which involves nuclear protein binding to the 5' E-box, was detected only with nuclear extracts from lymphoid cells. Specific antisera were used to show that the CD4-3A complex contains a heterodimer or heterooligomer of basic helix-loop-helix transcriptional factors, E12 or a related factor and HEB, which is expressed predominantly in thymus. Consistent with this finding, in vitro-translated E12 and HEB proteins, as homodimers or heterodimers, bound preferentially to the 5' E-box. Point mutations in the 5' E-box, but not in the 3' E-box, abolished CD4 enhancer activity. Furthermore, overexpression of Id, a protein that forms inactive heterodimers with E12/E47, blocked CD4 enhancer activity in T cells. These results suggest that a heterodimer composed of HEB and E12 or a closely related protein plays a critical role in CD4 enhancer function by interacting with the 5' E-box motif of the CD4-3 site in vivo.

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