scholarly journals Early specification of sensory neuron fate revealed by expression and function of neurogenins in the chick embryo

Development ◽  
1999 ◽  
Vol 126 (8) ◽  
pp. 1715-1728 ◽  
Author(s):  
S.E. Perez ◽  
S. Rebelo ◽  
D.J. Anderson
Keyword(s):  
Neural Crest ◽  
Sensory Neuron ◽  
Ectopic Expression ◽  
Neural Crest Cells ◽  
Sensory Ganglia ◽  
Helix Loop Helix ◽  
Autonomic Neurons ◽  
And Function ◽  
Bhlh Transcription Factors

The generation of sensory and autonomic neurons from the neural crest requires the functions of two classes of basic helix-loop-helix (bHLH) transcription factors, the Neurogenins (NGNs) and MASH-1, respectively (Fode, C., Gradwohl, G., Morin, X., Dierich, A., LeMeur, M., Goridis, C. and Guillemot, F. (1998) Neuron 20, 483–494; Guillemot, F., Lo, L.-C., Johnson, J. E., Auerbach, A., Anderson, D. J. and Joyner, A. L. (1993) Cell 75, 463–476; Ma, Q., Chen, Z. F., Barrantes, I. B., de la Pompa, J. L. and Anderson, D. J. (1998 Neuron 20, 469–482). We have cloned two chick NGNs and found that they are expressed in a subset of neural crest cells early in their migration. Ectopic expression of the NGNs in vivo biases migrating neural crest cells to localize in the sensory ganglia, and induces the expression of sensory neuron-appropriate markers in non-sensory crest derivatives. Surprisingly, the NGNs can also induce the expression of multiple pan-neuronal and sensory-specific markers in the dermomyotome, a mesodermal derivative. Taken together, these data suggest that a subset of neural crest cells may already be specified for a sensory neuron fate early in migration, as a consequence of NGN expression.

scholarly journals Identification of dividing, determined sensory neuron precursors in the mammalian neural crest

Development ◽  
1999 ◽  
Vol 126 (16) ◽  
pp. 3545-3559
Author(s):  
A.L. Greenwood ◽  
E.E. Turner ◽  
D.J. Anderson
Keyword(s):  
Transcription Factors ◽  
Neural Crest ◽  
Sensory Neurons ◽  
Large Diameter ◽  
Defined Medium ◽  
Culture Conditions ◽  
Helix Loop Helix ◽  
Pou Domain ◽  
Bhlh Transcription Factors

Sensory and autonomic neurons of the vertebrate peripheral nervous system are derived from the neural crest. Here we use the expression of lineage-specific transcription factors as a means to identify neuronal subtypes that develop in rat neural crest cultures grown in a defined medium. Sensory neurons, identified by expression of the POU-domain transcription factor Brn-3.0, develop from dividing precursors that differentiate within 2 days following emigration from the neural tube. Most of these precursors generate sensory neurons even when challenged with BMP2, a factor that induces autonomic neurogenesis in many other cells in the explants. Moreover, BMP2 fails to prevent expression of the sensory-specific basic helix-loop-helix (bHLH) transcription factors neurogenin1, neurogenin2 and neuroD, although it induces expression of the autonomic-specific bHLH factor MASH1 and the paired homeodomain factor Phox2a in other cells. These data suggest that there are mitotically active precursors in the mammalian neural crest that can generate sensory neurons even in the presence of a strong autonomic-inducing cue. Further characterization of the neurons generated from such precursors indicates that, under these culture conditions, they exhibit a proprioceptive and/or mechanosensory, but not nociceptive, phenotype. Such precursors may therefore correspond to a lineally (Frank, E. and Sanes, J. (1991) Development 111, 895–908) and genetically (Ma, Q., Fode, C., Guillemot, F. and Anderson, D. J. (1999) Genes Dev. 13, in press) distinct subset of early-differentiating precursors of large-diameter sensory neurons identified in vivo.

scholarly journals The vertebrate-specific VENTX/NANOG gene empowers neural crest with ectomesenchyme potential

2020 ◽  
Vol 6 (18) ◽  
pp. eaaz1469 ◽  
Author(s):  
Pierluigi Scerbo ◽  
Anne H. Monsoro-Burq
Keyword(s):  
Neural Crest ◽  
Sensory Neuron ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Pigment Cells ◽  
Regulatory State ◽  
Neural Plate Border ◽  
Nanog Gene ◽  
Neural Ectoderm

During Cambrian, unipotent progenitors located at the neural (plate) border (NB) of an Olfactoria chordate embryo acquired the competence to form ectomesenchyme, pigment cells and neurons, initiating the rise of the multipotent neural crest cells (NC) specific to vertebrates. Surprisingly, the known vertebrate NB/NC transcriptional circuitry is a constrained feature also found in invertebrates. Therefore, evidence for vertebrate-specific innovations endowing vertebrate NC with multipotency is still missing. Here, we identified VENTX/NANOG and POU5/OCT4 as vertebrate-specific innovations. When VENTX was depleted in vivo and in directly-induced NC, the NC lost its early multipotent state and its skeletogenic potential, but kept sensory neuron and pigment identity, thus reminiscent of invertebrate NB precursors. In vivo, VENTX gain-of-function enabled NB specifiers to reprogram embryonic non-neural ectoderm towards early NC identity. We propose that skeletogenic NC evolved by acquiring VENTX/NANOG activity, promoting a novel multipotent progenitor regulatory state into the pre-existing sensory neuron/pigment NB program.

Differentiation in vitro of sympathetic cells from chick embryo sensory ganglia

Development ◽  
1975 ◽  
Vol 33 (1) ◽  
pp. 43-56
Author(s):  
D. F. Newgreen ◽  
R. O. Jones
Keyword(s):  
Chick Embryo ◽  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Sensory Ganglia ◽  
Sensory Ganglion ◽  
Neural Crest Origin ◽  
Fluorescent Cells

This study was carried out in order to determine what factors control the differentiation of certain neural crest cells in the chick embryo. Emphasis was placed on the morphologically and biochemically divergent sensory and sympathetic pathways of differentiation. Embryos were precisely staged according to Hamburger & Hamilton (1951) and it was observed that sensory ganglia with somites, explanted at stages 21–24, gave rise to cells showing formaldehyde-induced fluorescence in more than 25% of explants. These cells were identical in properties to the fluorescent cells of the sympathetic system of embryos of similar age, and appeared by 12 days in vitro. These fluorescent cells did not appear when somites and sensory ganglia explants were maintained separately. The incidence of fluorescent cells in combined explants was considerably reduced or absent when cultures were maintained for 7 days or less, or when the explants were obtainedfrom stage 25–26 embryos. Furthermore, when neural tube was also included in the cultures, the appearance of fluorescent cells was markedly inhibited. The requirement for somitic tissue to induce fluorescent cells in combined explants can be replaced by forelimb-bud tissue. The origin of these cells and the factors that control their differentiation in vitro are discussed with reference to the neural crest origin of the sensory ganglion, and the possible conditions pertaining in vivo in this region.

Cell cycle of neural crest cells in the early migratory stage in vivo

1994 ◽  
Vol 27 (9) ◽  
pp. 571-578 ◽  
Author(s):  
M. G. Paglini ◽  
R. A. Rovasio
Keyword(s):  
Cell Cycle ◽  
Neural Crest ◽  
Neural Crest Cells

scholarly journals In Vivo Transplantation of Enteric Neural Crest Cells into Mouse Gut; Engraftment, Functional Integration and Long-Term Safety

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0147989 ◽  
Author(s):  
Julie E. Cooper ◽  
Conor J. McCann ◽  
Dipa Natarajan ◽  
Shanas Choudhury ◽  
Werend Boesmans ◽  
...  
Keyword(s):  
Neural Crest ◽  
Functional Integration ◽  
Neural Crest Cells

scholarly journals miR-135a Reduces Osteosarcoma Pulmonary Metastasis by Targeting Both BMI1 and KLF4

2021 ◽  
Vol 11 ◽  
Author(s):  
Chenglong Chen ◽  
Xingjia Mao ◽  
Caitong Cheng ◽  
Yurui Jiao ◽  
Yi Zhou ◽  
...  
Keyword(s):  
Cell Invasion ◽  
Tumor Recurrence ◽  
Response Rate ◽  
Ectopic Expression ◽  
Chemotherapy Treatment ◽  
Therapeutic Approaches ◽  
Inhibit Tumor Growth ◽  
And Function ◽  
Novel Therapeutic

Because of the modest response rate after surgery and chemotherapy, treatment of osteosarcoma (OS) remains challenging due to tumor recurrence and metastasis. miR-135a has been reported to act as an anticarcinogenic regulator of several cancers. However, its expression and function in osteosarcoma remain largely unknown. Here, we reported that abridged miR-135a expression in OS cells and tissues, and its expression is inversely correlated with the expression of BMI1 and KLF4, which are described as oncogenes in several cancers. Ectopic expression of miR-135a inhibited cell invasion and expression of BMI1 and KLF4 in OS cells. In vivo investigation confirmed that miR-135a acts as a tumor suppressor in OS to inhibit tumor growth and lung metastasis in xenograft nude mice. BMI1 and KLF4 were revealed to be direct targets of miR-135a, and miR-135a had a similar effect as the combination of si-BMI1 and si-KLF4 on inhibiting tumor progression and the expression of BMI1 and KLF4 in vivo. Altogether, our results demonstrate that the targeting of BMI1/KLF4 with miR-135a may provide an applicable strategy for exploring novel therapeutic approaches for OS.

scholarly journals Lineage-specific requirements of β-catenin in neural crest development

2002 ◽  
Vol 159 (5) ◽  
pp. 867-880 ◽  
Author(s):  
Lisette Hari ◽  
Véronique Brault ◽  
Maurice Kléber ◽  
Hye-Youn Lee ◽  
Fabian Ille ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neural Crest ◽  
Neural Crest Cells ◽  
Neural Crest Stem Cells ◽  
Downstream Signaling ◽  
Neural Crest Development ◽  
Sensory Neurogenesis

β-Catenin plays a pivotal role in cadherin-mediated cell adhesion. Moreover, it is a downstream signaling component of Wnt that controls multiple developmental processes such as cell proliferation, apoptosis, and fate decisions. To study the role of β-catenin in neural crest development, we used the Cre/loxP system to ablate β-catenin specifically in neural crest stem cells. Although several neural crest–derived structures develop normally, mutant animals lack melanocytes and dorsal root ganglia (DRG). In vivo and in vitro analyses revealed that mutant neural crest cells emigrate but fail to generate an early wave of sensory neurogenesis that is normally marked by the transcription factor neurogenin (ngn) 2. This indicates a role of β-catenin in premigratory or early migratory neural crest and points to heterogeneity of neural crest cells at the earliest stages of crest development. In addition, migratory neural crest cells lateral to the neural tube do not aggregate to form DRG and are unable to produce a later wave of sensory neurogenesis usually marked by the transcription factor ngn1. We propose that the requirement of β-catenin for the specification of melanocytes and sensory neuronal lineages reflects roles of β-catenin both in Wnt signaling and in mediating cell–cell interactions.

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