ArticlebioRxiv : the preprint server for biology2025
PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Spliceosomopathies, which are a group of disorders caused by defects in the splicing machinery, frequently affect the craniofacial skeleton and limb, but the molecular mechanism underlying this tissue-specific sensitivity remains unclear. Splicing factors and small nuclear ribonucleoproteins (snRNPs) are core components of splicing machinery, and splicing factors are further controlled by post-translational modifications, among which arginine methylation is one of the most prevalent. We determined the splicing mechanisms in the cranial neural crest cells (CNCCs), a multipotent developmental population that gives rise to the majority of the craniofacial skeleton, and focused on an upstream regulator of splicing proteins, protein arginine methyltransferase 1 (PRMT1). PRMT1 is the highest expressing arginine methyltransferase in CNCCs and its role in craniofacial development is evident from our earlier investigation, where CNCC-specific
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