ArticleDevelopment (Cambridge, England)2007
Fgf3 is required for dorsal patterning and morphogenesis of the inner ear epithelium.
Article in Development (Cambridge, England), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
60 citing papers in PubMed, 87 citations in OpenAlex.
- A Novel Missense Mutation in the FGF3 Gene of a Chinese Patient with LAMM Syndrome.Biochemical genetics · 2026Article
- Early and transient requirements for FGFR2b/1b ligands in cochlear sensory and neural cell subtype differentiation.Developmental biology · 2025Article
- Human organoids for rapid validation of gene variants linked to cochlear malformations.Human genetics · 2025Article
- Decoding FGF/FGFR Signaling: Insights into Biological Functions and Disease Relevance.Biomolecules · 2024Review
- Identification of a novel FGF3 variant and a new phenotype in three LAMM syndrome families.BMC medical genomics · 2024Article
- Human Organoids for Rapid Validation of Gene Variants Linked to Cochlear Malformations.Research square · 2024Article
- CHD7 and SOX2 act in a common gene regulatory network during mammalian semicircular canal and cochlear development.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Shared features in ear and kidney development - implications for oto-renal syndromes.Disease models & mechanisms · 2024Article
- Mapping oto-pharyngeal development in a human inner ear organoid model.Development (Cambridge, England) · 2023Article
- Fgf, Hh, and pax2a differentially regulate expression of pax5 and pou3f3b in vestibular and auditory maculae in the zebrafish otic vesicle.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Identification of a homozygous frameshift mutation in the FGF3 gene in a consanguineous Iranian family: First report of labyrinthine aplasia, microtia, and microdontia syndrome in Iran and literature review.Molecular genetics & genomic medicine · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Inactivation of Fgf3 and Fgf4 within the Fgf3/Fgf4/Fgf15 gene cluster reveals their redundant requirement for mouse inner ear induction and embryonic survival.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Knockout ofBiomedicines · 2021Article
- Comparative assessment of Fgf's diverse roles in inner ear development: A zebrafish perspective.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Review
- Lmx1a and Lmx1b are Redundantly Required for the Development of Multiple Components of the Mammalian Auditory System.Neuroscience · 2021Article
- A probabilistic atlas of the human inner ear's bony labyrinth enables reliable atlas-based segmentation of the total fluid space.Journal of neurology · 2019Article
- Article
- A requirement for Fgfr2 in middle ear development.Genesis (New York, N.Y. : 2000) · 2019Article
- Spatial and temporal inhibition of FGFR2b ligands reveals continuous requirements and novel targets in mouse inner ear morphogenesis.Development (Cambridge, England) · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The inner ear, which contains sensory organs specialized for hearing and balance, develops from an ectodermal placode that invaginates lateral to hindbrain rhombomeres (r) 5-6 to form the otic vesicle. Under the influence of signals from intra- and extraotic sources, the vesicle is molecularly patterned and undergoes morphogenesis and cell-type differentiation to acquire its distinct functional compartments. We show in mouse that Fgf3, which is expressed in the hindbrain from otic induction through endolymphatic duct outgrowth, and in the prospective neurosensory domain of the otic epithelium as morphogenesis initiates, is required for both auditory and vestibular function. We provide new morphologic data on otic dysmorphogenesis in Fgf3 mutants, which show a range of malformations similar to those of Mafb (Kreisler), Hoxa1 and Gbx2 mutants, the most common phenotype being failure of endolymphatic duct and common crus formation, accompanied by epithelial dilatation and reduced cochlear coiling. The malformations have close parallels with those seen in hearing-impaired patients. The morphologic data, together with an analysis of changes in the molecular patterning of Fgf3 mutant otic vesicles, and comparisons with other mutations affecting otic morphogenesis, allow placement of Fgf3 between hindbrain-expressed Hoxa1 and Mafb, and otic vesicle-expressed Gbx2, in the genetic cascade initiated by WNT signaling that leads to dorsal otic patterning and endolymphatic duct formation. Finally, we show that Fgf3 prevents ventral expansion of r5-6 neurectodermal Wnt3a, serving to focus inductive WNT signals on the dorsal otic vesicle and highlighting a new example of cross-talk between the two signaling systems.
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Registered trials
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.