ArticleDevelopment (Cambridge, England)2021
Sobp modulates the transcriptional activation of Six1 target genes and is required during craniofacial development.
Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- SIX1 branchio-oto-renal syndrome variants have different effects on embryonic craniofacial gene expression and cartilage formation.Development (Cambridge, England) · 2026Article
- A Five-Gene Signature for the Prediction of Event-Free Survival of Both Pediatric and Adult Acute Myeloid Leukemia.Diagnostics (Basel, Switzerland) · 2025Article
- Targets of the transcription factor Six1 identify previously unreported candidate deafness genes.Development (Cambridge, England) · 2025Article
- Long-term expandable mouse and human-induced nephron progenitor cells enable kidney organoid maturation and modeling of plasticity and disease.Cell stem cell · 2024Article
- Using Xenopus to discover new candidate genes involved in BOR and other congenital hearing loss syndromes.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2024Review
- Novel likely pathogenic variant in the EYA1 gene causing Branchio oto renal syndrome and the exploration of pathogenic mechanisms.BMC medical genomics · 2024Article
- Bop1 is required to establish precursor domains of craniofacial tissues.Genesis (New York, N.Y. : 2000) · 2024Article
- Mechanisms of pathogenicity and the quest for genetic modifiers of kidney disease in branchiootorenal syndrome.Clinical kidney journal · 2024Article
- Transcriptomic analysis reveals the role of SIX1 in mouse cranial neural crest patterning and bone development.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Phenotypic and molecular basis of SIX1 variants linked to non-syndromic deafness and atypical branchio-otic syndrome in South Korea.Scientific reports · 2023Article
- Retinal determination gene networks: from biological functions to therapeutic strategies.Biomarker research · 2023Review
- Zmym4 is required for early cranial gene expression and craniofacial cartilage formation.Frontiers in cell and developmental biology · 2023Article
- Six1 promotes skeletal muscle thyroid hormone response through regulation of the MCT10 transporter.Skeletal muscle · 2021Article
- Deep learning is widely applicable to phenotyping embryonic development and disease.Development (Cambridge, England) · 2021Article
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Authors and funding
5 authors.
Funding
Abstract
Branchio-oto-renal syndrome (BOR) is a disorder characterized by hearing loss, and craniofacial and/or renal defects. Variants in the transcription factor Six1 and its co-factor Eya1, both of which are required for otic development, are linked to BOR. We previously identified Sobp as a potential Six1 co-factor, and SOBP variants in mouse and humans cause otic phenotypes; therefore, we asked whether Sobp interacts with Six1 and thereby may contribute to BOR. Co-immunoprecipitation and immunofluorescence experiments demonstrate that Sobp binds to and colocalizes with Six1 in the cell nucleus. Luciferase assays show that Sobp interferes with the transcriptional activation of Six1+Eya1 target genes. Experiments in Xenopus embryos that either knock down or increase expression of Sobp show that it is required for formation of ectodermal domains at neural plate stages. In addition, altering Sobp levels disrupts otic vesicle development and causes craniofacial cartilage defects. Expression of Xenopus Sobp containing the human variant disrupts the pre-placodal ectoderm similar to full-length Sobp, but other changes are distinct. These results indicate that Sobp modifies Six1 function and is required for vertebrate craniofacial development, and identify Sobp as a potential candidate gene for BOR.
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