ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2025
Human stem cell model of neural crest cell differentiation reveals a requirement of SF3B4 in survival, maintenance, and differentiation.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Epigenomic regulation of neural crest differentiation in human-induced pluripotent stem cells.iScience · 2026Article
- Modelling Acral Melanoma in Admixed Brazilians Uncovers Genomic Drivers and Targetable Pathways.medRxiv : the preprint server for health sciences · 2025Article
- Modeling craniofacial spliceosomopathies: a pathway toward deciphering disease mechanisms.Frontiers in cell and developmental biology · 2025Review
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Abstract
backgroundIn vitro modeling is a powerful approach to investigate the pathomechanisms driving human congenital conditions. Here, we use human embryonic stem cells (hESCs) to model Nager and Rodriguez syndromes, two craniofacial conditions characterized by hypoplastic neural crest-derived craniofacial bones, caused by pathogenic variants of SF3B4, a core component of the spliceosome.
resultsWe observed that siRNA-mediated knockdown of SF3B4 interferes with the production of hESC-derived neural crest cells, as seen by a marked reduction in neural crest gene expression. This phenotype is associated with an increase in neural crest cell apoptosis and premature neuronal differentiation.
conclusionsAltogether, these results point to a role of SF3B4 in neural crest cell survival, maintenance, and differentiation. We propose that the dysregulation of these processes may contribute to Nager/Rodriguez syndrome-associated craniofacial defects.
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