ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2025
Expression analysis of genes including Zfhx4 in mice and zebrafish reveals a temporospatial conserved molecular basis underlying craniofacial development.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Next-Generation Sequencing Data and Clinical Features in Patients with Cleft Palate and Tooth Agenesis: A Systematic Literature Review.Dentistry journal · 2026Review
- Chemical-induced heart defects using a transgenic zebrafish model.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Novel Genetic Variants and Clinical Profiles in Peters Anomaly Spectrum Disorders.International journal of molecular sciences · 2025Article
- Expression analysis of genes including Zfhx4 in mice and zebrafish reveals a temporospatial conserved molecular basis underlying craniofacial development.Developmental dynamics : an official publication of the American Association of Anatomists · 2025Article
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17 authors.
Funding
Abstract
backgroundEmbryonic craniofacial development involves several cellular and molecular events that are evolutionarily conserved among vertebrates. Vertebrate models such as mice and zebrafish have been used to investigate the molecular and cellular etiologies underlying human craniofacial disorders, including orofacial clefts. However, the molecular mechanisms underlying embryonic development in these two species are unknown. Therefore, elucidating the shared mechanisms of craniofacial development between disease models is crucial to understanding the underlying mechanisms of phenotypes in individual species.
resultsWe selected mice and zebrafish as model organisms to compare various events during embryonic craniofacial development. We identified genes (Sox9, Zfhx3 and 4, Cjun, and Six1) exhibiting similar temporal expression patterns between these species through comprehensive and stage-matched gene expression analyses. Expression analysis revealed similar gene expression in hypothetically corresponding tissues, such as the mice palate and zebrafish ethmoid plate. Furthermore, loss-of-function analysis of Zfhx4/zfhx4, a causative gene of human craniofacial anomalies including orofacial cleft, in both species resulted in deformed skeletal elements such as the palatine and ethmoid plate in mice and zebrafish, respectively.
conclusionsThese results demonstrate that these disease models share common molecular mechanisms, highlighting their usefulness in modeling craniofacial defects in humans.
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