scholarly journals Neuromesodermal Progenitor Origin of Trunk Neural Crest in vivo

2021 ◽  
Author(s):  
Martyna Lukoseviciute ◽  
Sarah Mayes ◽  
Tatjana Sauka-Spengler
Keyword(s):  
Neural Crest ◽  
Trunk Neural Crest

scholarly journals In Vivo Quantitative Imaging Provides Insights into Trunk Neural Crest Migration

Cell Reports ◽  
2019 ◽  
Vol 26 (6) ◽  
pp. 1489-1500.e3 ◽  
Author(s):  
Yuwei Li ◽  
Felipe M. Vieceli ◽  
Walter G. Gonzalez ◽  
Ang Li ◽  
Weiyi Tang ◽  
...  
Keyword(s):  
Neural Crest ◽  
Quantitative Imaging ◽  
Trunk Neural Crest ◽  
Neural Crest Migration

scholarly journals PuraMatrix allows differentiation of a broad repertoire of neural and mesenchymal phenotypes from trunk neural crest

2020 ◽  
Vol 64 (7-8-9) ◽  
pp. 433-443
Author(s):  
Clarissa R. Taufer ◽  
Monica A. Rodrigues-Da-Silva ◽  
Giordano W. Calloni
Keyword(s):  
Neural Crest ◽  
Mesenchymal Cell ◽  
Cell Types ◽  
Full Potential ◽  
Self Renewal ◽  
Mesenchymal Differentiation ◽  
Trunk Neural Crest ◽  
And Control

The neural crest (NC) is a transitory embryonic structure of vertebrates that gives rise to an astonishing variety of derivatives, encompassing both neural and mesenchymal cell types. Neural crest cells (NCCs) are an excellent model to study how environmental factors modulate features such as cell multipotentiality and differentiation. Tests with multifunctional substrates that allow NCCs to express their full potential, while promoting cell subcloning, are needed to advance knowledge about NCC self-renewal and to foster future biotechnological approaches. Here we show that a self-assembled peptide named PuraMatrixTM is an excellent substrate that allows the differentiation of NCCs based on the identification of seven different cell types. Depending on the PuraMatrixTM concentration employed, different frequencies and quantities of a given cell type were obtained. It is noteworthy that an enormous quantity and diversity of mesenchymal phenotypes, such as chondrocytes, could be observed. The quantity of adipocytes and osteocytes also increased with the use of mesenchymal differentiation factors (MDF), but PuraMatrixTM alone can support the appearance of these mesenchymal cell types. PuraMatrixTM will promote advances in studies related to multipotentiality, self-renewal and control of NCC differentiation, since it is an extremely simple and versatile material which can be employed for both in vivo and in vitro experiments.

scholarly journals Neuromesodermal progenitor origin of trunk neural crest in vivo

2021 ◽  
Author(s):  
Martyna Lukoseviciute ◽  
Sarah Mayes ◽  
Tatjana Sauka-Spengler
Keyword(s):  
Neural Crest ◽  
Single Cell Analysis ◽  
Neuronal Cell ◽  
Cell Types ◽  
Neural Cells ◽  
Embryonic Cells ◽  
Cell Fates ◽  
Trunk Neural Crest ◽  
Bona Fide

AbstractNeural crest (NC) is a vertebrate-specific population of multipotent embryonic cells predisposed to particular derivatives along the anteroposterior (A-P) axis. While only cranial NC progenitors give rise to ectomesenchymal cell types, trunk NC is biased for neuronal cell fates. By integrating multimodal single-cell analysis we uncovered heterogenous NC cells across the entire A-P axis expressing NC regulator foxd3. We pinpointed to its specific cranial and trunk auto-regulated enhancers. The trunk foxd3 enhancer, however, did not mark the bona fide NC, but bipotent tailbud neuromesodermal progenitors (NMps). A subset of these NMp-derived pro-neural cells appeared to give rise to neuronal trunk NC in amniotes in vivo, suggesting that at least a portion of trunk NC progenitors with a bias for neuronal fates originated from NMps in vivo.

scholarly journals Dual function of Slit2 in repulsion and enhanced migration of trunk, but not vagal, neural crest cells

2003 ◽  
Vol 162 (2) ◽  
pp. 269-279 ◽  
Author(s):  
Maria Elena De Bellard ◽  
Yi Rao ◽  
Marianne Bronner-Fraser
Keyword(s):  
Neural Crest ◽  
Neural Crest Cells ◽  
Dual Function ◽  
In Vitro Experiments ◽  
Enteric Ganglia ◽  
Robo Receptors ◽  
Trunk Neural Crest ◽  
Differential Ability

Neural crest precursors to the autonomic nervous system form different derivatives depending upon their axial level of origin; for example, vagal, but not trunk, neural crest cells form the enteric ganglia of the gut. Here, we show that Slit2 is expressed at the entrance of the gut, which is selectively invaded by vagal, but not trunk, neural crest. Accordingly, only trunk neural crest cells express Robo receptors. In vivo and in vitro experiments demonstrate that trunk, not vagal, crest cells avoid cells or cell membranes expressing Slit2, thereby contributing to the differential ability of neural crest populations to invade and innervate the gut. Conversely, exposure to soluble Slit2 significantly increases the distance traversed by trunk neural crest cells. These results suggest that Slit2 can act bifunctionally, both repulsing and stimulating the motility of trunk neural crest cells.

scholarly journals Cancer-associated HIF-2α impacts trunk neural crest stemness

2020 ◽  
Author(s):  
Sofie Mohlin ◽  
Camilla U. Persson ◽  
Elina Fredlund ◽  
Emanuela Monni ◽  
Jessica M. Lindvall ◽  
...  
Keyword(s):  
Neural Crest ◽  
Normal Development ◽  
Hypoxia Inducible Factor ◽  
Neural Crest Cells ◽  
Sympathetic Ganglia ◽  
Stem Cell Population ◽  
Neural Crest Development ◽  
Trunk Neural Crest

AbstractThe neural crest is a stem cell population that gives rise to sympathetic ganglia, the cell type of origin of neuroblastoma. Hypoxia Inducible Factor (HIF)-2α is associated with high risk neuroblastoma, however, little is known about its role in normal neural crest development. To address this important question, here we show that HIF-2α is expressed in trunk neural crest cells of human, murine and avian embryos. Modulating HIF-2α in vivo not only causes developmental delays but also induces proliferation and stemness of neural crest cells while altering the number of cells migrating ventrally to sympathoadrenal sites. Transcriptome changes after loss of HIF-2α reflect the in vivo phenotype. The results suggest that expression levels of HIF-2α must be strictly controlled and abnormal levels increase stemness and may promote metastasis. Our findings help elucidate the role of HIF-2α during normal development with implications also in tumor initiation at the onset of neuroblastoma.

scholarly journals Regulation of sarcomagenesis by the empty spiracles homeobox genes EMX1 and EMX2

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Manuel Pedro Jimenez-García ◽  
Antonio Lucena-Cacace ◽  
Daniel Otero-Albiol ◽  
Amancio Carnero
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Transcription Factors ◽  
Neural Crest ◽  
Tumor Suppressors ◽  
Homeobox Genes ◽  
Neuronal Cell ◽  
Cell Gene Expression

AbstractThe EMX (Empty Spiracles Homeobox) genes EMX1 and EMX2 are two homeodomain gene members of the EMX family of transcription factors involved in the regulation of various biological processes, such as cell proliferation, migration, and differentiation, during brain development and neural crest migration. They play a role in the specification of positional identity, the proliferation of neural stem cells, and the differentiation of certain neuronal cell phenotypes. In general, they act as transcription factors in early embryogenesis and neuroembryogenesis from metazoans to higher vertebrates. The EMX1 and EMX2’s potential as tumor suppressor genes has been suggested in some cancers. Our work showed that EMX1/EMX2 act as tumor suppressors in sarcomas by repressing the activity of stem cell regulatory genes (OCT4, SOX2, KLF4, MYC, NANOG, NES, and PROM1). EMX protein downregulation, therefore, induced the malignance and stemness of cells both in vitro and in vivo. In murine knockout (KO) models lacking Emx genes, 3MC-induced sarcomas were more aggressive and infiltrative, had a greater capacity for tumor self-renewal, and had higher stem cell gene expression and nestin expression than those in wild-type models. These results showing that EMX genes acted as stemness regulators were reproduced in different subtypes of sarcoma. Therefore, it is possible that the EMX genes could have a generalized behavior regulating proliferation of neural crest-derived progenitors. Together, these results indicate that the EMX1 and EMX2 genes negatively regulate these tumor-altering populations or cancer stem cells, acting as tumor suppressors in sarcoma.

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