Evidence map›Paper›PMID 33554859›Full record

ArticleeLife2021

TWIST1 and chromatin regulatory proteins interact to guide neural crest cell differentiation.

Xiaochen Fan, V Pragathi Masamsetti, Jane Qj Sun, Kasper Engholm-Keller, Pierre Osteil, Joshua Studdert, Mark E Graham, Nicolas Fossat, Patrick Pl Tam

Abstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

  1. Article
  2. A dual role for GLI3 signaling in neural crest development.Development (Cambridge, England) · 2026
    Article
  3. eLife · 2025
    Article
  4. Review
  5. bioRxiv : the preprint server for biology · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Epithelial-mesenchymal transition in tissue repair and degeneration.Nature reviews. Molecular cell biology · 2024
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Xiaochen FanEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.ORCID 0000-0002-4316-0616
V Pragathi MasamsettiEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Jane Qj SunEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Kasper Engholm-KellerSynapse Proteomics Group, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Pierre OsteilEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Joshua StuddertEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Mark E GrahamSynapse Proteomics Group, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.ORCID 0000-0002-7290-1217
Nicolas FossatEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Patrick Pl TamEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.ORCID 0000-0001-6950-8388

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein interaction is critical molecular regulatory activity underlining cellular functions and precise cell fate choices. Using TWIST1 BioID-proximity-labeling and network propagation analyses, we discovered and characterized a TWIST-chromatin regulatory module (TWIST1-CRM) in the neural crest cells (NCC). Combinatorial perturbation of core members of TWIST1-CRM: TWIST1, CHD7, CHD8, and WHSC1 in cell models and mouse embryos revealed that loss of the function of the regulatory module resulted in abnormal differentiation of NCCs and compromised craniofacial tissue patterning. Following NCC delamination, low level of TWIST1-CRM activity is instrumental to stabilize the early NCC signatures and migratory potential by repressing the neural stem cell programs. High level of TWIST1 module activity at later phases commits the cells to the ectomesenchyme. Our study further revealed the functional interdependency of TWIST1 and potential neurocristopathy factors in NCC development.

Indexed as

Cell DifferentiationAnimalsChromatinEmbryonic Stem CellsMiceNeural CrestTwist-Related Protein 1ChromatinTwist1 protein, mouseTwist-Related Protein 1cell biologycraniofacial developmentdevelopmental biologyectomesenchymemouseneural stem cellneurocristopathyneurodevelopmentproteomics

Identifiers

PMID33554859
PMCPMC7968925

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.