Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (674 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The two longitudinal ridges along the primitive streak appearing near the end of gastrulation during development of nervous system (neurulation). The ridges are formed by folding of neural plate. Between the ridges is a neural groove which deepens as the fold become elevated. When the folds meet at midline, the groove becomes a closed tube, the neural tube.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Crest, Neural; Crests, Neural; Neural Crests; Neural Fold; Fold, Neural; Folds, Neural; Neural Folds; Neural Groove.
Where it fits in the MeSH classification
- Broader topics
- Embryonic Structures
Related concepts
- Primitive Streak
- Gastrulation
- Neurulation
- Neural Plate
- Neural Tube
Research landscape
PubMed indexes 7,319 records tagged with the MeSH heading “Neural Crest” (counts retrieved 2026-10-31). 1,158 of them (15.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 2,212 records.
Reviews account for 1,287 records (17.6%) and meta-analyses for 3. Randomized controlled trials number 0 (0.0%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 2,052 |
| 2000-2009 | 1,897 |
| 2010-2019 | 2,212 |
| 2020 onward | 1,158 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 1,287 | 17.6% |
| Meta-analyses | 3 | 0.0% |
| Randomized controlled trials | 0 | 0.0% |
Method: PubMed query "Neural Crest"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Loss of Extreme Long-Range Enhancers in Human Neural Crest Drives a Craniofacial Disorder | 2020 | Research article Design not recorded in structured metadata | 172 | cc by PMID 32991838 · DOI · PMC7655526 |
| Schwann cell precursors represent a neural crest-like state with biased multipotency | 2022 | Research article Design not recorded in structured metadata | 117 | cc by PMID 35815410 · DOI · PMC9434083 |
| Spatiotemporal single-cell regulatory atlas reveals neural crest lineage diversification and cellular function during tooth morphogenesis | 2022 | Research article Design not recorded in structured metadata | 98 | cc by PMID 35974052 · DOI · PMC9381504 |
| Eed controls craniofacial osteoblast differentiation and mesenchymal proliferation from the neural crest | 2025 | Research article Design not recorded in structured metadata | 2 | cc by PMID 41329158 · DOI · PMC12671911 |
Loss of Extreme Long-Range Enhancers in Human Neural Crest Drives a Craniofacial Disorder [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Non-coding mutations at the far end of a large gene desert surrounding the SOX9 gene result in a human craniofacial disorder called Pierre Robin sequence (PRS).
- Closing excerpt
- Overall, we characterize the longest-range human enhancers involved in congenital malformations, directly demonstrate that PRS is an enhanceropathy, and illustrate how small changes in gene expression can lead to morphological variation.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Non-coding mutations at the far end of a large gene desert surrounding the SOX9 gene result in a human craniofacial disorder called Pierre Robin sequence (PRS). Leveraging a human stem cell differentiation model, we identify two clusters of enhancers within the PRS-associated region that regulate SOX9 expression during a restricted window of facial progenitor development at distances up to 1.45 Mb. Enhancers within the 1.45 Mb cluster exhibit highly synergistic activity that is dependent on the Coordinator motif. Using mouse models, we demonstrate that PRS phenotypic specificity arises from the convergence of two mechanisms: confinement of Sox9 dosage perturbation to developing facial structures through context-specific enhancer activity and heightened sensitivity of the lower jaw to Sox9 expression reduction. Overall, we characterize the longest-range human enhancers involved in congenital malformations, directly demonstrate that PRS is an enhanceropathy, and illustrate how small changes in gene expression can lead to morphological variation.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32991838 · DOI · PMC7655526
Schwann cell precursors represent a neural crest-like state with biased multipotency [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Schwann cell precursors (SCPs) are nerve-associated progenitors that can generate myelinating and non-myelinating Schwann cells but also are multipotent like the neural crest cells from which they originate.
- Closing excerpt
- Overall, SCPs resemble migrating neural crest cells that maintain multipotency and become transcriptionally primed towards distinct lineages.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (177 words)
Schwann cell precursors (SCPs) are nerve-associated progenitors that can generate myelinating and non-myelinating Schwann cells but also are multipotent like the neural crest cells from which they originate. SCPs are omnipresent along outgrowing peripheral nerves throughout the body of vertebrate embryos. By using single-cell transcriptomics to generate a gene expression atlas of the entire neural crest lineage, we show that early SCPs and late migratory crest cells have similar transcriptional profiles characterised by a multipotent "hub" state containing cells biased towards traditional neural crest fates. SCPs keep diverging from the neural crest after being primed towards terminal Schwann cells and other fates, with different subtypes residing in distinct anatomical locations. Functional experiments using CRISPR-Cas9 loss-of-function further show that knockout of the common "hub" gene Sox8 causes defects in neural crest-derived cells along peripheral nerves by facilitating differentiation of SCPs towards sympathoadrenal fates. Finally, specific tumour populations found in melanoma, neurofibroma and neuroblastoma map to different stages of SCP/Schwann cell development. Overall, SCPs resemble migrating neural crest cells that maintain multipotency and become transcriptionally primed towards distinct lineages.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35815410 · DOI · PMC9434083
Spatiotemporal single-cell regulatory atlas reveals neural crest lineage diversification and cellular function during tooth morphogenesis [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Cranial neural crest cells are an evolutionary innovation of vertebrates for craniofacial development and function, yet the mechanisms that govern the cell fate decisions of postmigratory cranial neural crest cells remain largely unknown.
- Closing excerpt
- Our single-cell atlas provides comprehensive mechanistic insight into the cell fate diversification process of the cranial neural crest cell-derived odontogenic populations.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (159 words)
Cranial neural crest cells are an evolutionary innovation of vertebrates for craniofacial development and function, yet the mechanisms that govern the cell fate decisions of postmigratory cranial neural crest cells remain largely unknown. Using the mouse molar as a model, we perform single-cell transcriptome profiling to interrogate the cell fate diversification of postmigratory cranial neural crest cells. We reveal the landscape of transcriptional heterogeneity and define the specific cellular domains during the progression of cranial neural crest cell-derived dental lineage diversification, and find that each domain makes a specific contribution to distinct molar mesenchymal tissues. Furthermore, IGF signaling-mediated cell-cell interaction between the cellular domains highlights the pivotal role of autonomous regulation of the dental mesenchyme. Importantly, we reveal cell-type-specific gene regulatory networks in the dental mesenchyme and show that Foxp4 is indispensable for the differentiation of periodontal ligament. Our single-cell atlas provides comprehensive mechanistic insight into the cell fate diversification process of the cranial neural crest cell-derived odontogenic populations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35974052 · DOI · PMC9381504
Eed controls craniofacial osteoblast differentiation and mesenchymal proliferation from the neural crest [4]
Abstract reading summary — source excerpts
- Opening excerpt
- The histone methyltransferase Polycomb repressive complex 2 (PRC2) is required for specification of the neural crest, and mis-regulation of neural crest development can cause severe congenital malformations.
- Closing excerpt
- These data enhance understanding of epigenetic mechanisms that underlie craniofacial development and shed light on the embryonic, cellular, and molecular drivers of rare congenital syndromes in humans.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (189 words)
The histone methyltransferase Polycomb repressive complex 2 (PRC2) is required for specification of the neural crest, and mis-regulation of neural crest development can cause severe congenital malformations. PRC2 is necessary for neural crest induction, but the embryonic, cellular, and molecular consequences of PRC2 activity after neural crest induction are incompletely understood. Here, we show that Eed, which encodes a protein that is a core subunit of PRC2, is required for craniofacial osteoblast differentiation and mesenchymal proliferation after induction of the neural crest. Integrating mouse genetics with single-cell RNA sequencing and epigenetic profiling, our results reveal that conditional knockout of Eed after neural crest cell induction causes severe craniofacial hypoplasia, impaired craniofacial osteogenesis, and attenuated craniofacial mesenchymal cell proliferation that is first evident in post-migratory neural crest cell populations. We show that Eed drives mesenchymal differentiation and proliferation in vivo and in primary craniofacial cell cultures by epigenetically regulating diverse transcription factor programs that are required for specification of post-migratory neural crest cells. These data enhance understanding of epigenetic mechanisms that underlie craniofacial development and shed light on the embryonic, cellular, and molecular drivers of rare congenital syndromes in humans.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41329158 · DOI · PMC12671911
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Establishing neural crest identity: a gene regulatory recipe [5]
- Research article Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development [6]
- Research article Cranial neural crest and the building of the vertebrate head [7]
- Research article Development and evolution of the neural crest: an overview [8]
- Research article Neuroblastoma: molecular pathogenesis and therapy [9]
- Research article The neural crest [10]
References
- Long HK, Osterwalder M, Welsh IC, Hansen K, Davies JOJ, Liu YE, et al.. Loss of Extreme Long-Range Enhancers in Human Neural Crest Drives a Craniofacial Disorder. . 2020. PMID 32991838 · DOI · PMC7655526
- Kastriti ME, Faure L, Von Ahsen D, Bouderlique TG, Boström J, Solovieva T, et al.. Schwann cell precursors represent a neural crest-like state with biased multipotency. . 2022. PMID 35815410 · DOI · PMC9434083
- Jing J, Feng J, Yuan Y, Guo T, Lei J, Pei F, et al.. Spatiotemporal single-cell regulatory atlas reveals neural crest lineage diversification and cellular function during tooth morphogenesis. . 2022. PMID 35974052 · DOI · PMC9381504
- Casey-Clyde T, Liu SJ, Pelonero A, Serrano JAC, Teng C, Jang YG, et al.. Eed controls craniofacial osteoblast differentiation and mesenchymal proliferation from the neural crest. . 2025. PMID 41329158 · DOI · PMC12671911
- Simões-Costa M, Bronner ME. Establishing neural crest identity: a gene regulatory recipe. Development. 2015. PMID 25564621 · DOI · PMC4302844
- Minoux M, Rijli FM. Molecular mechanisms of cranial neural crest cell migration and patterning in craniofacial development. Development. 2010. PMID 20663816 · DOI
- Santagati F, Rijli FM. Cranial neural crest and the building of the vertebrate head. Nat Rev Neurosci. 2003. PMID 14523380 · DOI
- Bronner ME, LeDouarin NM. Development and evolution of the neural crest: an overview. Dev Biol. 2012. PMID 22230617 · DOI · PMC3351559
- Louis CU, Shohet JM. Neuroblastoma: molecular pathogenesis and therapy. Annu Rev Med. 2015. PMID 25386934 · DOI · PMC4418018
- Mayor R, Theveneau E. The neural crest. Development. 2013. PMID 23674598 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
See how EvidenceLib is built. Spotted an error? Email support@evidencehelix.com.
Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.