ArticleDevelopment (Cambridge, England)2002
Eya1 is required for the morphogenesis of mammalian thymus, parathyroid and thyroid.
Article in Development (Cambridge, England), 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.
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Who cites it
99 citing papers in PubMed, 282 citations in OpenAlex.
- Article
- SIX1 branchio-oto-renal syndrome variants have different effects on embryonic craniofacial gene expression and cartilage formation.Development (Cambridge, England) · 2026Article
- From renal biopsy to genetic diagnosis: EYA1 mutation in branchio-oto-renal syndrome with renal insufficiency.BMC nephrology · 2025Article
- Branchio-oto-renal syndrome in a young Han Chinese female: a case report and review of the literature.Journal of medical case reports · 2025Review
- An iPSC-based in vitro model recapitulates human thymic epithelial development and multi-lineage specification.Nature communications · 2025Article
- Generation of parathyroid glands from pluripotent stem cells.Endocrine journal · 2025Review
- IPSC-induced podocytes from a BORS patient with EYA1 gene mutation showed glucocorticoid-resistant and cytoskeletal rearrangement.Cellular and molecular life sciences : CMLS · 2025Article
- Targets of the transcription factor Six1 identify previously unreported candidate deafness genes.Development (Cambridge, England) · 2025Article
- Review of the Pathophysiology and Clinical Manifestations of 22q11.2 Deletion and Duplication Syndromes.Clinical reviews in allergy & immunology · 2025Review
- Thyroid C-Cell Biology and Oncogenic Transformation.Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer · 2025Review
- Protein phosphatase EYA1 regulates the dephosphorylation and turnover of BCL2L12 to promote glioma development.International journal of biological sciences · 2025Article
- Thymus Ontogeny and Development.Advances in experimental medicine and biology · 2025Review
- A pre-vertebrate endodermal origin of calcitonin-producing neuroendocrine cells.Development (Cambridge, England) · 2024Article
- Novel likely pathogenic variant in the EYA1 gene causing Branchio oto renal syndrome and the exploration of pathogenic mechanisms.BMC medical genomics · 2024Article
- In Vitro Phosphatase Assays for the Eya2 Tyrosine Phosphatase.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Generation and molecular characterization of human pluripotent stem cell-derived pharyngeal foregut endoderm.Developmental cell · 2023Article
- Pre-mandibular pharyngeal pouches in early non-teleost fish embryos.Proceedings. Biological sciences · 2023Article
- Cellular and molecular mechanisms of the organogenesis and development, and function of the mammalian parathyroid gland.Cell and tissue research · 2023Review
- Stem Cell Bioengineering with Bioportides: Inhibition of Planarian Head Regeneration with Peptide Mimetics of Eyes Absent Proteins.Pharmaceutics · 2023Article
- Case report: A novel mutation in the EYA1 gene in a child with branchiootic syndrome with secretory otitis media and bilateral vestibular hypofunction.Frontiers in genetics · 2023Article
39 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Eyes absent (Eya) genes regulate organogenesis in both vertebrates and invertebrates. Mutations in human EYA1 cause congenital Branchio-Oto-Renal (BOR) syndrome, while targeted inactivation of murine Eya1 impairs early developmental processes in multiple organs, including ear, kidney and skeletal system. We have now examined the role of Eya1 during the morphogenesis of organs derived from the pharyngeal region, including thymus, parathyroid and thyroid. The thymus and parathyroid are derived from 3rd pharyngeal pouches and their development is initiated via inductive interactions between neural crest-derived arch mesenchyme, pouch endoderm, and possibly the surface ectoderm of 3rd pharyngeal clefts. Eya1 is expressed in all three cell types during thymus and parathyroid development from E9.5 and the organ primordia for both of these structures failed to form in Eya1(-/-) embryos. These results indicate that Eya1 is required for the initiation of thymus and parathyroid gland formation. Eya1 is also expressed in the 4th pharyngeal region and ultimobranchial bodies. Eya1(-/-) mice show thyroid hypoplasia, with severe reduction in the number of parafollicular cells and the size of the thyroid lobes and lack of fusion between the ultimobranchial bodies and the thyroid lobe. These data indicate that Eya1 also regulates mature thyroid gland formation. Furthermore, we show that Six1 expression is markedly reduced in the arch mesenchyme, pouch endoderm and surface ectoderm in the pharyngeal region of Eya1(-/-) embryos, indicating that Six1 expression in those structures is Eya1 dependent. In addition, we show that in Eya1(-/-) embryos, the expression of Gcm2 in the 3rd pouch endoderm is undetectable at E10.5, however, the expression of Hox and Pax genes in the pouch endoderm is preserved at E9.5-10.5. Finally, we found that the surface ectoderm of the 3rd and 4th pharyngeal region show increased cell death at E10.5 in Eya1(-/-) embryos. Our results indicate that Eya1 controls critical early inductive events involved in the morphogenesis of thymus, parathyroid and thyroid.
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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 OpenQuestion graph.