ArticleNature communications2025
PRMT1-methylated MSX1 phase separates to control palate development.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- A Comprehensive Review of the Genetic Etiology and Management of Orofacial Clefts.Pediatric discovery · 2026Review
- Phase separation of OPTN initiates mitophagy to orchestrate craniofacial bone mineralization.Autophagy · 2026Article
- OGT mediates O-GlcNAcylation of MEIS2 and affects palatal osteogenic development.International journal of oral science · 2026Article
- TDRD3, a Tudor domain-containing protein, regulatesScience advances · 2026Article
- The regulatory principles, physiological functions, and phase transition of biomolecular condensates.Frontiers in cell and developmental biology · 2026Review
- Multi-Omics and Clinical Data Analyses of Protein Arginine Methyltransferases in Pan-Cancer and Colorectal Cancer.International journal of medical sciences · 2026Article
- Alternative Splicing: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
Little is known about the regulation and function of phase separation in craniofacial developmental disorders. MSX1 mutations are associated with human cleft palate, the most common craniofacial birth defect. Here, we show that MSX1 phase separation is a vertebrate-conserved mechanism underlying embryonic palatal fusion. Notably, MSX1 phase separation is triggered by its intrinsically disordered protein region (IDR) and regulated by PRMT1-catalyzed methylation, specifically asymmetric dimethylation of arginine in the MSX1 IDR including R150 and R157. Hypomethylated MSX1 due to methylation site mutations and PRMT1 deficiency consistently leads to abnormal MSX1 phase separation to form less dynamic gel-like condensates, resulting in proliferation defects of embryonic palatal mesenchymal cells and cleft palate. Besides, high frequency mutations in the MSX1 IDR, especially R157S, have been identified in humans with cleft palate. Overall, we reveal the function and regulatory pathway of MSX1 phase separation as a conserved mechanism underlying cleft palate, providing a proof-of-concept example of a phenotype-associated phase separation mechanism associated with craniofacial developmental disorders.
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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 Socratic graph.