ArticleDevelopment (Cambridge, England)2022
PRDM paralogs antagonistically balance Wnt/β-catenin activity during craniofacial chondrocyte differentiation.
Article in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- A Human Accelerated Region Drives Opposing Heterochronic Changes in Craniofacial and Limb Development.bioRxiv : the preprint server for biology · 2026Article
- Piezo channels contribute to the terminal cytodifferentiation of odontoblasts via modulation of canonical Wnt signaling.International journal of oral science · 2026Article
- Combinatorial multiomic analysis from a pedigree of Sox10Dom Hirschsprung mice identifies multiple high confidence candidate modifiers of Enteric Nervous System development.PLoS computational biology · 2026Article
- PRDM Family Proteins in Immune Regulation: Epigenetic Control and Implications in Immune-Related Diseases.Biology · 2026Review
- PRDM paralogs are required for Meckel's cartilage formation during mandibular bone development.Developmental biology · 2026Article
- CXXC Finger Protein 1 drives BMP signaling and progenitor cell differentiation during limb development.Developmental biology · 2025Article
- Combinatorial multiomic analysis from a pedigree of Sox10bioRxiv : the preprint server for biology · 2025Article
- PRDM16 functions as a co-repressor in the BMP pathway to suppress neural stem cell proliferation.eLife · 2025Article
- A zinc finger-dependent, PRDM13-driven mechanism regulates retinal progenitor cell fate from mouse embryonic stem cells via WNT signaling.Stem cell reports · 2025Article
- Article
- PRDM16 Enhances Osteoblastogenic RUNX2 via Canonical WNT10b/β-CATENIN Pathway in Testosterone-Treated Hypogonadal Men.Biomolecules · 2025Article
- β-catenin Orchestrates Gli1+ Cell Fate in Condylar Development and TMJOA.Journal of dental research · 2024Article
- Epigenetic regulation of craniofacial development and disease.Birth defects research · 2024Review
- Genome-wide association study for growth traits with 1066 individuals in largemouth bass (Frontiers in molecular biosciences · 2024Article
- PRDM3/16 Regulate Chromatin Accessibility Required for NKX2-1 Mediated Alveolar Epithelial Differentiation and Function.bioRxiv : the preprint server for biology · 2023Article
- Nonsense Variant PRDM16-Q187X Causes Impaired Myocardial Development and TGF-β Signaling Resulting in Noncompaction Cardiomyopathy in Humans and Mice.Circulation. Heart failure · 2023Article
- The Tumor SuppressorJournal of developmental biology · 2023Article
- Facial analytics based on a coordinate extrapolation system (zFACE) for morphometric phenotyping of developing zebrafish.Disease models & mechanisms · 2023Article
- Overexpression ofAmerican journal of undergraduate research · 2023Article
- PRDM1 DNA-binding zinc finger domain is required for normal limb development and is disrupted in split hand/foot malformation.Disease models & mechanisms · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Cranial neural crest cell (NCC)-derived chondrocyte precursors undergo a dynamic differentiation and maturation process to establish a scaffold for subsequent bone formation, alterations in which contribute to congenital birth defects. Here, we demonstrate that transcription factor and histone methyltransferase proteins Prdm3 and Prdm16 control the differentiation switch of cranial NCCs to craniofacial cartilage. Loss of either paralog results in hypoplastic and disorganized chondrocytes due to impaired cellular orientation and polarity. We show that these proteins regulate cartilage differentiation by controlling the timing of Wnt/β-catenin activity in strikingly different ways: Prdm3 represses whereas Prdm16 activates global gene expression, although both act by regulating Wnt enhanceosome activity and chromatin accessibility. Finally, we show that manipulating Wnt/β-catenin signaling pharmacologically or generating prdm3-/-;prdm16-/- double mutants rescues craniofacial cartilage defects. Our findings reveal upstream regulatory roles for Prdm3 and Prdm16 in cranial NCCs to control Wnt/β-catenin transcriptional activity during chondrocyte differentiation to ensure proper development of the craniofacial skeleton.
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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.