Cellular and molecular aspects of cephalic neural crest development: workshop report

Development ◽  
1988 ◽  
Vol 103 (Supplement) ◽  
pp. 95-99
Author(s):  
Jim Bee ◽  
Don Newgreen
Keyword(s):  
Neural Crest ◽  
Cell Types ◽  
Neural Plate ◽  
Facial Skeleton ◽  
Workshop Report ◽  
Neural Crest Development ◽  
Organ Systems ◽  
Molecular Aspects ◽  
Unique Cell ◽  
Anterior Posterior

The neural crest (NC) is derived from the ectoderm at the lateral borders of the neural plate and is first distinct during the later stages of neurulation when prospective NC cells segregate from the surrounding epidermal ectoderm and neurectoderm along the entire dorsolateral aspect of the forming and newly formed neural tube. From this origin, NC cells migrate extensive distances throughout the embryo to give rise to a large number of differentiated cell types and contribute to a diverse series of organ systems. This unique cell population therefore poses fundamental questions of the mechanisms underlying morphogenesis and differentiation during embryonic development. The developmental fate of NC cells reflects their point of origin along the anterior–posterior axis of the embryo. Of particular significance to the present volume is the major contribution of cells derived from the cephalic NC to the facial skeleton.

scholarly journals Xenopus Nkx6.3 Is a Neural Plate Border Specifier Required for Neural Crest Development

PLoS ONE ◽  
2014 ◽  
Vol 9 (12) ◽  
pp. e115165 ◽  
Author(s):  
Zuming Zhang ◽  
Yu Shi ◽  
Shuhua Zhao ◽  
Jiejing Li ◽  
Chaocui Li ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Plate ◽  
Neural Crest Development ◽  
Neural Plate Border

scholarly journals Bimodal function of chromatin remodeler Hmga1 in neural crest induction and Wnt-dependent emigration

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Shashank Gandhi ◽  
Erica J Hutchins ◽  
Krystyna Maruszko ◽  
Jong H Park ◽  
Matthew Thomson ◽  
...  
Keyword(s):  
Neural Crest ◽  
Neural Tube ◽  
Neural Crest Cells ◽  
Neural Plate ◽  
Chromatin Remodeler ◽  
Lineage Specification ◽  
Dorsal Neural Tube ◽  
Neural Crest Development ◽  
Neural Plate Border ◽  
Canonical Wnt

During gastrulation, neural crest cells are specified at the neural plate border, as characterized by Pax7 expression. Using single-cell RNA sequencing coupled with high-resolution in situ hybridization to identify novel transcriptional regulators, we show that chromatin remodeler Hmga1 is highly expressed prior to specification and maintained in migrating chick neural crest cells. Temporally controlled CRISPR-Cas9-mediated knockouts uncovered two distinct functions of Hmga1 in neural crest development. At the neural plate border, Hmga1 regulates Pax7-dependent neural crest lineage specification. At premigratory stages, a second role manifests where Hmga1 loss reduces cranial crest emigration from the dorsal neural tube independent of Pax7. Interestingly, this is rescued by stabilized ß-catenin, thus implicating Hmga1 as a canonical Wnt activator. Together, our results show that Hmga1 functions in a bimodal manner during neural crest development to regulate specification at the neural plate border, and subsequent emigration from the neural tube via canonical Wnt signaling.

scholarly journals Single-Cell Multiomic Approaches Reveal Diverse Labeling of the Nervous System by Common Cre-Drivers

2021 ◽  
Vol 15 ◽  
Author(s):  
Rachel A. Keuls ◽  
Ronald J. Parchem
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Single Cell ◽  
System Development ◽  
Cell Types ◽  
Nervous System Development ◽  
Cellular Heterogeneity ◽  
Cranial Neural Crest ◽  
Developmental Potential ◽  
Neural Crest Development

Neural crest development involves a series of dynamic, carefully coordinated events that result in human disease when not properly orchestrated. Cranial neural crest cells acquire unique multipotent developmental potential upon specification to generate a broad variety of cell types. Studies of early mammalian neural crest and nervous system development often use the Cre-loxP system to lineage trace and mark cells for further investigation. Here, we carefully profile the activity of two common neural crest Cre-drivers at the end of neurulation in mice. RNA sequencing of labeled cells at E9.5 reveals that Wnt1-Cre2 marks cells with neuronal characteristics consistent with neuroepithelial expression, whereas Sox10-Cre predominantly labels the migratory neural crest. We used single-cell mRNA and single-cell ATAC sequencing to profile the expression of Wnt1 and Sox10 and identify transcription factors that may regulate the expression of Wnt1-Cre2 in the neuroepithelium and Sox10-Cre in the migratory neural crest. Our data identify cellular heterogeneity during cranial neural crest development and identify specific populations labeled by two Cre-drivers in the developing nervous system.

scholarly journals Tumor Necrosis Factor-Receptor–associated Factor-4 Is a Positive Regulator of Transforming Growth Factor-β Signaling That Affects Neural Crest Formation

2009 ◽  
Vol 20 (14) ◽  
pp. 3436-3450 ◽  
Author(s):  
Tuzer Kalkan ◽  
Yasuno Iwasaki ◽  
Chong Yon Park ◽  
Gerald H. Thomsen
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Neural Crest ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Neural Plate ◽  
Nodal Signaling ◽  
Associated Factor ◽  
Neural Crest Development ◽  
Necrosis Factor

The transforming growth factor (TGF)-β superfamily regulates cell proliferation, apoptosis, differentiation, migration, and development. Canonical TGFβ signals are transduced to the nucleus via Smads in both major signaling branches, bone morphogenetic protein (BMP) or Activin/Nodal/TGFβ. Smurf ubiquitin (Ub) ligases attenuate these pathways by targeting Smads and other signaling components for degradation by the 26S proteasome. Here, we identify tumor necrosis factor (TNF)-receptor–associated factor-4 (TRAF4) as a new target of Smurf1, which polyubiquitylates TRAF4 to trigger its proteasomal destruction. Unlike other TRAF family members, which mediate signal transduction by TNF, interleukin, or Toll-like receptors, we find that TRAF4 potentiates BMP and Nodal signaling. In the frog Xenopus laevis, TRAF4 mRNA is stored maternally in the egg animal pole, and in the embryo it is expressed in the gastrula marginal zone, neural plate, and cranial and trunk neural crest. Knockdown of embryonic TRAF4 impairs signaling, neural crest development and neural folding, whereas TRAF4 overexpression boosts signaling and expands the neural crest. In human embryonic kidney 293 cells, small interfering RNA knockdown of Smurf1 elevates TRAF4 levels, indicating endogenous regulation of TRAF4 by Smurf1. Our results uncover new functions for TRAF4 as a Smurf1-regulated mediator of BMP and Nodal signaling that are essential for neural crest development and neural plate morphogenesis.

scholarly journals Wnt Signaling in Neural Crest Ontogenesis and Oncogenesis

Cells ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 1173 ◽  
Author(s):  
Yu Ji ◽  
Hongyan Hao ◽  
Kurt Reynolds ◽  
Moira McMahon ◽  
Chengji J. Zhou
Keyword(s):  
Embryonic Development ◽  
Wnt Signaling ◽  
Neural Crest ◽  
Cell Types ◽  
Multipotent Stem Cells ◽  
Peripheral Neurons ◽  
Dorsal Edge ◽  
Cell Induction ◽  
Vertebrate Embryos ◽  
Anterior Posterior

Neural crest (NC) cells are a temporary population of multipotent stem cells that generate a diverse array of cell types, including craniofacial bone and cartilage, smooth muscle cells, melanocytes, and peripheral neurons and glia during embryonic development. Defective neural crest development can cause severe and common structural birth defects, such as craniofacial anomalies and congenital heart disease. In the early vertebrate embryos, NC cells emerge from the dorsal edge of the neural tube during neurulation and then migrate extensively throughout the anterior-posterior body axis to generate numerous derivatives. Wnt signaling plays essential roles in embryonic development and cancer. This review summarizes current understanding of Wnt signaling in NC cell induction, delamination, migration, multipotency, and fate determination, as well as in NC-derived cancers.

The zebrafish colourless gene regulates development of non-ectomesenchymal neural crest derivatives

Development ◽  
2000 ◽  
Vol 127 (3) ◽  
pp. 515-525 ◽  
Author(s):  
R.N. Kelsh ◽  
J.S. Eisen
Keyword(s):  
Nervous System ◽  
Neural Crest ◽  
Cell Types ◽  
Pigment Cells ◽  
Specific Cell ◽  
Zebrafish Embryos ◽  
Craniofacial Skeleton ◽  
Cell Fates ◽  
Peripheral Neurons ◽  
Neural Crest Development

Neural crest forms four major categories of derivatives: pigment cells, peripheral neurons, peripheral glia, and ectomesenchymal cells. Some early neural crest cells generate progeny of several fates. How specific cell fates become specified is still poorly understood. Here we show that zebrafish embryos with mutations in the colourless gene have severe defects in most crest-derived cell types, including pigment cells, neurons and specific glia. In contrast, craniofacial skeleton and medial fin mesenchyme are normal. These observations suggest that colourless has a key role in development of non-ectomesenchymal neural crest fates, but not in development of ectomesenchymal fates. Thus, the cls mutant phenotype reveals a segregation of ectomesenchymal and non-ectomesenchymal fates during zebrafish neural crest development. The combination of pigmentation and enteric nervous system defects makes colourless mutations a model for two human neurocristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.

Delta signaling mediates segregation of neural crest and spinal sensory neurons from zebrafish lateral neural plate

Development ◽  
2000 ◽  
Vol 127 (13) ◽  
pp. 2873-2882 ◽  
Author(s):  
R.A. Cornell ◽  
J.S. Eisen
Keyword(s):  
Neural Crest ◽  
Point Mutation ◽  
Sensory Neurons ◽  
Genetic Difference ◽  
Neural Plate ◽  
Cranial Neural Crest ◽  
Neural Crest Development ◽  
Neural Crest Derivative ◽  
Trunk Neural Crest

We examined the role of Delta signaling in specification of two derivatives in zebrafish neural plate: Rohon-Beard spinal sensory neurons and neural crest. deltaA-expressing Rohon-Beard neurons are intermingled with premigratory neural crest cells in the trunk lateral neural plate. Embryos homozygous for a point mutation in deltaA, or with experimentally reduced delta signalling, have supernumerary Rohon-Beard neurons, reduced trunk-level expression of neural crest markers and lack trunk neural crest derivatives. Fin mesenchyme, a putative trunk neural crest derivative, is present in deltaA mutants, suggesting it segregates from other neural crest derivatives as early as the neural plate stage. Cranial neural crest derivatives are also present in deltaA mutants, revealing a genetic difference in regulation of trunk and cranial neural crest development.

scholarly journals Biphasic influence of Miz1 on neural crest development by regulating cell survival and apical adhesion complex formation in the developing neural tube

2014 ◽  
Vol 25 (3) ◽  
pp. 347-355 ◽  
Author(s):  
Laura Kerosuo ◽  
Marianne E. Bronner
Keyword(s):  
Neural Crest ◽  
Cell Survival ◽  
Neural Tube ◽  
Zinc Finger Protein ◽  
Critical Role ◽  
Neural Plate ◽  
Neural Crest Development ◽  
Finger Protein ◽  
Neural Plate Border ◽  
Adhesion Complex

Myc interacting zinc finger protein-1 (Miz1) is a transcription factor known to regulate cell cycle– and cell adhesion–related genes in cancer. Here we show that Miz1 also plays a critical role in neural crest development. In the chick, Miz1 is expressed throughout the neural plate and closing neural tube. Its morpholino-mediated knockdown affects neural crest precursor survival, leading to reduction of neural plate border and neural crest specifier genes Msx-1, Pax7, FoxD3, and Sox10. Of interest, Miz1 loss also causes marked reduction of adhesion molecules (N-cadherin, cadherin6B, and α1-catenin) with a concomitant increase of E-cadherin in the neural folds, likely leading to delayed and decreased neural crest emigration. Conversely, Miz1 overexpression results in up-regulation of cadherin6B and FoxD3 expression in the neural folds/neural tube, leading to premature neural crest emigration and increased number of migratory crest cells. Although Miz1 loss effects cell survival and proliferation throughout the neural plate, the neural progenitor marker Sox2 was unaffected, suggesting a neural crest–selective effect. The results suggest that Miz1 is important not only for survival of neural crest precursors, but also for maintenance of integrity of the neural folds and tube, via correct formation of the apical adhesion complex therein.

scholarly journals ADAR1 mediated regulation of neural crest derived melanocytes and Schwann cell development

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Nadjet Gacem ◽  
Anthula Kavo ◽  
Lisa Zerad ◽  
Laurence Richard ◽  
Stephane Mathis ◽  
...  
Keyword(s):  
Neural Crest ◽  
Schwann Cells ◽  
Peripheral Nerves ◽  
Cell Types ◽  
Interferon Stimulated Genes ◽  
Conditional Deletion ◽  
Neural Crest Development ◽  
Numerous Cell ◽  
Schwann Cell Development

AbstractThe neural crest gives rise to numerous cell types, dysfunction of which contributes to many disorders. Here, we report that adenosine deaminase acting on RNA (ADAR1), responsible for adenosine-to-inosine editing of RNA, is required for regulating the development of two neural crest derivatives: melanocytes and Schwann cells. Neural crest specific conditional deletion of Adar1 in mice leads to global depigmentation and absence of myelin from peripheral nerves, resulting from alterations in melanocyte survival and differentiation of Schwann cells, respectively. Upregulation of interferon stimulated genes precedes these defects, which are associated with the triggering of a signature resembling response to injury in peripheral nerves. Simultaneous extinction of MDA5, a key sensor of unedited RNA, rescues both melanocytes and myelin defects in vitro, suggesting that ADAR1 safeguards neural crest derivatives from aberrant MDA5-mediated interferon production. We thus extend the landscape of ADAR1 function to the fields of neural crest development and disease.

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