ArticleDevelopmental biology2014
Ephrin-B2 governs morphogenesis of endolymphatic sac and duct epithelia in the mouse inner ear.
Article in Developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Molecular Characterization of Subdomain Specification of Cochlear Duct Based on Foxg1 and Gata3.International journal of molecular sciences · 2024Article
- Prenatal diagnosis of distal 13q deletion syndrome in a fetus with esophageal atresia: a case report and review of the literature.Journal of medical case reports · 2022Review
- SOX9 and SOX10 control fluid homeostasis in the inner ear for hearing through independent and cooperative mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Genetic architecture and phenotypic landscape of SLC26A4-related hearing loss.Human genetics · 2022Review
- Development and evolution of the vestibular apparatuses of the inner ear.Journal of anatomy · 2021Review
- Single-Cell Sequencing Applications in the Inner Ear.Frontiers in cell and developmental biology · 2021Review
- Digenic inheritance of mutations in EPHA2 and SLC26A4 in Pendred syndrome.Nature communications · 2020Article
- Age-related transcriptome changes in Sox2+ supporting cells in the mouse cochlea.Stem cell research & therapy · 2019Article
- Immunolocalization of calcium sensing and transport proteins in the murine endolymphatic sac indicates calciostatic functions within the inner ear.Cell and tissue research · 2019Article
- Approaches for the study of epigenetic modifications in the inner ear and related tissues.Hearing research · 2019Review
- Reciprocal Negative Regulation Between Lmx1a and Lmo4 Is Required for Inner Ear Formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
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- Ephrin-B/EphB Signaling Is Required for Normal Innervation of Lingual Gustatory Papillae.Developmental neuroscience · 2016Article
- The mouse Foxi3 transcription factor is necessary for the development of posterior placodes.Developmental biology · 2016Article
- The cochlear sensory epithelium derives from Wnt responsive cells in the dorsomedial otic cup.Developmental biology · 2015Article
- The role of foxi family transcription factors in the development of the ear and jaw.Current topics in developmental biology · 2015Review
- Pou3f4-mediated regulation of ephrin-b2 controls temporal bone development in the mouse.PloS one · 2014Article
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Authors and funding
6 authors at 4 institutions in 3 countries.
Funding
Abstract
Control over ionic composition and volume of the inner ear luminal fluid endolymph is essential for normal hearing and balance. Mice deficient in either the EphB2 receptor tyrosine kinase or the cognate transmembrane ligand ephrin-B2 (Efnb2) exhibit background strain-specific vestibular-behavioral dysfunction and signs of abnormal endolymph homeostasis. Using various loss-of-function mouse models, we found that Efnb2 is required for growth and morphogenesis of the embryonic endolymphatic epithelium, a precursor of the endolymphatic sac (ES) and duct (ED), which mediate endolymph homeostasis. Conditional inactivation of Efnb2 in early-stage embryonic ear tissues disrupted cell proliferation, cell survival, and epithelial folding at the origin of the endolymphatic epithelium. This correlated with apparent absence of an ED, mis-localization of ES ion transport cells relative to inner ear sensory organs, dysplasia of the endolymph fluid space, and abnormally formed otoconia (extracellular calcite-protein composites) at later stages of embryonic development. A comparison of Efnb2 and Notch signaling-deficient mutant phenotypes indicated that these two signaling systems have distinct and non-overlapping roles in ES/ED development. Homozygous deletion of the Efnb2 C-terminus caused abnormalities similar to those found in the conditional Efnb2 null homozygote. Analyses of fetal Efnb2 C-terminus deletion heterozygotes found mis-localized ES ion transport cells only in the genetic background exhibiting vestibular dysfunction. We propose that developmental dysplasias described here are a gene dose-sensitive cause of the vestibular dysfunction observed in EphB-Efnb2 signaling-deficient mice.
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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.