ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2023
Transcriptomic analysis reveals the role of SIX1 in mouse cranial neural crest patterning and bone development.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 6 citations in OpenAlex.
- Developmentally relevant proteins contribute to chemotherapeutic resistance in neuroblastoma.Frontiers in oncology · 2026Review
- Non-recurrent duplications on chromosome 4p16.1 involving cis-regulatory elements affecting neural crest development in patients with isolated bilateral microtia.Human genetics · 2025Article
- Spatiotemporal Molecular Architecture of Lineage Allocation and Cellular Organization in Tooth Morphogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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5 authors at 3 institutions in 1 country.
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Abstract
backgroundGenetic variants of the transcription factor SIX1 and its co-factor EYA1 underlie 50% of Branchio-oto-renal syndrome (BOR) cases. BOR is characterized by craniofacial defects, including malformed middle ear ossicles leading to conductive hearing loss. In this work, we expand our knowledge of the Six1 gene regulatory network by using a Six1-null mouse line to assess gene expression profiles of E10.5 mandibular arches, which give rise to the neural crest (NC)-derived middle ear ossicles and lower jaw, via bulk RNA sequencing.
resultsOur transcriptomic analysis led to the identification of 808 differentially expressed genes that are related to translation, NC cell differentiation, osteogenesis, and chondrogenesis including components of the WNT signaling pathway. As WNT signaling is a known contributor to bone development, we demonstrated that SIX1 is required for expression of the WNT antagonist Frzb in the mandibular arch, and determined that SIX1 expression results in repression of WNT signaling.
conclusionOur results clarify the mechanisms by which SIX1 regulates the development of NC-derived craniofacial elements that are altered in SIX1-associated disorders. In addition, this work identifies novel genes that could be causative to this birth defect and establishes a link between SIX1 and WNT signaling during patterning of NC cells.
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