ArticleNature communications2026
NR6A1 is essential for neural crest cell specification, formation and survival.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Cranial neural crest shortage leads to extensive craniofacial anomalies in mice mutant for the NR2F1/2 nuclear receptors.Developmental biology · 2026Article
- A dual role for GLI3 signaling in neural crest development.Development (Cambridge, England) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
Neural crest cells (NCC) are a migratory progenitor cell population unique to vertebrates that contribute to nearly every organ system throughout the body. Disruptions in NCC development can result in congenital disorders (neurocristopathies). Yet, our understanding of the cellular mechanisms and signals that govern mammalian NCC formation remains poor. Here, we discovered nuclear receptor superfamily 6 group member 1 (NR6A1/GCNF/RTR) is a novel, critical regulator of mammalian NCC specification, formation and survival. Nr6a1 expression in mouse embryos spatiotemporally overlaps with early NCC development. NR6A1 loss-of-function perturbs anterior cranial NCC formation and survival, with complete agenesis of migratory NCC caudal to the first pharyngeal arch. Using targeted molecular and genomic approaches, we demonstrate that these phenotypes are associated with perturbation of NCC specification and epithelial-mesenchymal transition, and with persistent expression of pluripotency-associated factors. Supporting these observations, in vivo overexpression of Oct4 in gastrulating mouse embryos disrupts NCC specification and formation. Conditional temporal deletion revealed that Nr6a1 is required during mid-late gastrulation, demonstrating that the initiation of murine NCC specification likely occurs during gastrulation - earlier than previously thought, but in close alignment with the established timeline of NCC development in other vertebrate model organisms. These findings also reveal that the gold standard transgenic mouse line, Wnt1-Cre, is unsuitable for studying genetic function during NCC specification and formation. In summary, NR6A1 is essential for mammalian NCC development and may function during gastrulation as a bimodal switch modulating pluripotency-associated factors in the neuroepithelium, while concomitantly activating NCC specifiers and regulators of EMT.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.