scholarly journals Using Xenopus Neural Crest Explants to Study Epithelial-Mesenchymal Transition

2020 ◽  
pp. 257-274 ◽  
Author(s):  
Nadège Gouignard ◽  
Christian Rouvière ◽  
Eric Theveneau
Keyword(s):  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition

scholarly journals EMT-Inducing Transcription Factors, Drivers of Melanoma Phenotype Switching, and Resistance to Treatment

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2154 ◽  
Author(s):  
Yaqi Tang ◽  
Simon Durand ◽  
Stéphane Dalle ◽  
Julie Caramel
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Expression Patterns ◽  
Specific Expression ◽  
Therapeutic Targeting ◽  
Mesenchymal Transition ◽  
Neural Crest Stem Cell ◽  
Resistance To Treatment ◽  
Phenotype Switching

Transcription factors, extensively described for their role in epithelial–mesenchymal transition (EMT-TFs) in epithelial cells, also display essential functions in the melanocyte lineage. Recent evidence has shown specific expression patterns and functions of these EMT-TFs in neural crest-derived melanoma compared to carcinoma. Herein, we present an update of the specific roles of EMT-TFs in melanocyte differentiation and melanoma progression. As major regulators of phenotype switching between differentiated/proliferative and neural crest stem cell-like/invasive states, these factors appear as major drivers of intra-tumor heterogeneity and resistance to treatment in melanoma, which opens new avenues in terms of therapeutic targeting.

Transcription factor c-Myb is involved in the regulation of the epithelial-mesenchymal transition in the avian neural crest

2005 ◽  
Vol 62 (21) ◽  
pp. 2516-2525 ◽  
Author(s):  
V. Karafiat† ◽  
M. Dvorakova† ◽  
E. Krejci ◽  
J. Kralova ◽  
P. Pajer ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Factor C

scholarly journals Dullard-mediated Smad1/5/8 inhibition controls mouse cardiac neural crest cells condensation and outflow tract septation

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jean-François Darrigrand ◽  
Mariana Valente ◽  
Glenda Comai ◽  
Pauline Martinez ◽  
Maxime Petit ◽  
...  
Keyword(s):  
Neural Crest ◽  
Developmental Process ◽  
Epithelial Mesenchymal Transition ◽  
Neural Crest Cells ◽  
Systemic Circulation ◽  
Outflow Tract ◽  
Fine Tuning ◽  
Mesenchymal Transition ◽  
Bmp Signalling ◽  
Gradient Amplitude

The establishment of separated pulmonary and systemic circulation in vertebrates, via cardiac outflow tract (OFT) septation, is a sensitive developmental process accounting for 10% of all congenital anomalies. Neural Crest Cells (NCC) colonising the heart condensate along the primitive endocardial tube and force its scission into two tubes. Here, we show that NCC aggregation progressively decreases along the OFT distal-proximal axis following a BMP signalling gradient. Dullard, a nuclear phosphatase, tunes the BMP gradient amplitude and prevents NCC premature condensation. Dullard maintains transcriptional programs providing NCC with mesenchymal traits. It attenuates the expression of the aggregation factor Sema3c and conversely promotes that of the epithelial-mesenchymal transition driver Twist1. Altogether, Dullard-mediated fine-tuning of BMP signalling ensures the timed and progressive zipper-like closure of the OFT by the NCC and prevents the formation of a heart carrying the congenital abnormalities defining the tetralogy of Fallot.

scholarly journals FGF and retinoic acid activity gradients control the timing of neural crest cell emigration in the trunk

2011 ◽  
Vol 194 (3) ◽  
pp. 489-503 ◽  
Author(s):  
Patricia L. Martínez-Morales ◽  
Ruth Diez del Corral ◽  
Isabel Olivera-Martínez ◽  
Alejandra C. Quiroga ◽  
Raman M. Das ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Neural Crest Cell ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Mesenchymal Transition ◽  
Morphogenetic Protein ◽  
Trunk Neural Crest ◽  
Crest Cell

Coordination between functionally related adjacent tissues is essential during development. For example, formation of trunk neural crest cells (NCCs) is highly influenced by the adjacent mesoderm, but the molecular mechanism involved is not well understood. As part of this mechanism, fibroblast growth factor (FGF) and retinoic acid (RA) mesodermal gradients control the onset of neurogenesis in the extending neural tube. In this paper, using gain- and loss-of-function experiments, we show that caudal FGF signaling prevents premature specification of NCCs and, consequently, premature epithelial–mesenchymal transition (EMT) to allow cell emigration. In contrast, rostrally generated RA promotes EMT of NCCs at somitic levels. Furthermore, we show that FGF and RA signaling control EMT in part through the modulation of elements of the bone morphogenetic protein and Wnt signaling pathways. These data establish a clear role for opposition of FGF and RA signaling in control of the timing of NCC EMT and emigration and, consequently, coordination of the development of the central and peripheral nervous system during vertebrate trunk elongation.

scholarly journals p53 coordinates cranial neural crest cell growth and epithelial-mesenchymal transition/delamination processes

Development ◽  
2011 ◽  
Vol 138 (9) ◽  
pp. 1827-1838 ◽  
Author(s):  
A. Rinon ◽  
A. Molchadsky ◽  
E. Nathan ◽  
G. Yovel ◽  
V. Rotter ◽  
...  
Keyword(s):  
Cell Growth ◽  
Neural Crest ◽  
Epithelial Mesenchymal Transition ◽  
Neural Crest Cell ◽  
Cranial Neural Crest ◽  
Mesenchymal Transition ◽  
Cranial Neural Crest Cell ◽  
Crest Cell
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