{
  "id": 9137050,
  "title": "PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development",
  "url": "https://urgent.news/2026/09/22/prmt1-sfpq-regulates-intron-retention-to-control-matrix-gene",
  "topic": "science",
  "section": "Science",
  "published": "2026-09-22T00:00:00.000Z",
  "source": {
    "name": "eLife",
    "slug": "elife",
    "url": "https://elifesciences.org/articles/101386"
  },
  "original_language": "en",
  "account": "Spliceopathies, which stem from splicing machinery defects, often impact the craniofacial skeleton and limbs, yet the specific mechanism behind this tissue-specific vulnerability remains elusive. Splicing factors and small nuclear ribonucleoproteins (snRNPs) are essential components of the splicing machinery, with splicing factors being further regulated by post-translational modifications. Among these modifications, arginine methylation stands out as one of the most prevalent. Researchers have examined the splicing mechanisms in cranial neural crest cells (CNCCs), a versatile developmental population responsible for forming most of the craniofacial skeleton. They focused on an upstream regulator of splicing proteins, protein arginine methyltransferase 1 (PRMT1). PRMT1, the most abundant arginine methyltransferase in CNCCs, is pivotal in craniofacial development, as evidenced by earlier studies showing that Prmt1 deletion in CNCCs resulted in cleft palate and reduced mandibular size. PRMT1 functions by catalyzing arginine methylation of splicing factors, influencing protein localization, expression, and activity. This study reveals the role of PRMT1 in regulating intron retention, a form of alternative splicing where introns remain in the mature mRNA. CNCCs from the mandibular primordium of Prmt1-deficient embryos exhibited an increase in intron-retaining mRNA of matrix genes, leading to nonsense-mediated decay (NMD). This process reduced matrix mRNA levels. The study identified SFPQ as a PRMT1 substrate, crucial for arginine methylation and protein expression in developing craniofacial structures. Depletion of SFPQ in CNCCs mirrored PRMT1 deletion outcomes, demonstrating higher intron retention and lower expression in matrix, Wnt signaling, and neuronal genes. Moreover, the study noted that gene length was a common characteristic among SFPQ-regulated genes in CNCCs. These findings collectively demonstrate that the PRMT1-SFPQ pathway modulates matrix gene expression via intron retention-triggered NMD in CNCCs during craniofacial development.",
  "summary": "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…",
  "key_points": [],
  "editors_take": null,
  "illustration": null,
  "coverage": {
    "outlets": 1,
    "also_reported_by": []
  },
  "ai_generated": true,
  "disclaimer": "Summaries, key points and the editor’s take are written by software from other outlets’ reporting and may contain errors — always check the linked original."
}