PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development.
- Open access
PRMT1-SFPQ pathway controls intron retention to regulate matrix gene expression during craniofacial development, impacting tissue-specific splicing in CNCCs.
- Why it matters: Understanding tissue-specific sensitivity in splicing machinery defects is crucial for addressing splicing-related craniofacial disorders, which often involve intron retention issues.
- What they did: Researchers examined splicing mechanisms in cranial neural crest cells, focusing on PRMT1's role in modulating intron retention and its substrate SFPQ, through genetic and molecular analyses.
- The result: Findings reveal that PRMT1-mediated methylation of SFPQ influences intron retention and matrix gene expression, offering insights into molecular pathways critical for proper craniofacial development.