ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2026
Heterozygous Med13l mice recapitulate a developmental growth delay and craniofacial anomalies seen in MED13L syndrome.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Editorial highlights.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
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6 authors.
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Abstract
backgroundGene transcription is crucial for embryo and postnatal development and is regulated by the Mediator complex. Mediator is comprised of four submodules, including the kinase submodule (CKM). The CKM consists of MED13, MED12, CDK8, and CCNC. In mammals, there are paralogs for CKM components, including MED13L, MED12L, and CDK19. Neurological disorders have been associated with mutations in CKM genes including MED13L syndrome. MED13L syndrome is generally characterized as a haploinsufficiency of MED13L with a broad phenotypic response due in part to a wide range of de novo mutations.
resultsWe developed a Med13l heterozygous (HET) mouse model with an exon 11 deletion to evaluate whether Med13l HET mice are a viable research tool to study human phenotypes. We characterized our mouse model using growth, cardiovascular, and skeletal readouts. We observed Med13l HET mice are smaller than wildtype (WT) littermates, and over 60% of them exhibited one of two craniofacial anomalies: a pug snout with midface hypoplasia or a crooked snout. We also observed discontinuous squamosal sutures in a subset of our Med13l HETs.
conclusionsMed13l HET mice recapitulate MED13L syndrome phenotypes including a developmental growth delay and craniofacial anomalies. Med13l HET mice represent a novel research tool for MED13L syndrome.
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