Journal article
EphB2 Guides Axons at the Midline and Is Necessary for Normal Vestibular Function
Neuron (Cambridge, Mass.), Vol.26(2), pp.417-430
2000
DOI: 10.1016/S0896-6273(00)81174-5
PMID: 10839360
Abstract
Mice lacking the EphB2 receptor tyrosine kinase display a cell-autonomous, strain-specific circling behavior that is associated with vestibular phenotypes. In mutant embryos, the contralateral inner ear efferent growth cones exhibit inappropriate pathway selection at the midline, while in mutant adults, the endolymph-filled lumen of the semicircular canals is severely reduced. EphB2 is expressed in the endolymph-producing dark cells in the inner ear epithelium, and these cells show ultrastructural defects in the mutants. A molecular link to fluid regulation is provided by demonstrating that PDZ domain–containing proteins that bind the C termini of EphB2 and B-ephrins can also recognize the cytoplasmic tails of anion exchangers and aquaporins. This suggests EphB2 may regulate ionic homeostasis and endolymph fluid production through macromolecular associations with membrane channels that transport chloride, bicarbonate, and water.
Details
- Title: Subtitle
- EphB2 Guides Axons at the Midline and Is Necessary for Normal Vestibular Function
- Creators
- Chad A Cowan - Center for Developmental Biology and, Kent Waldrep Foundation Center for Basic Neuroscience Research, University of Texas, Southwestern Medical Center, Dallas, Texas 75235, USANobuhiko Yokoyama - Center for Developmental Biology and, Kent Waldrep Foundation Center for Basic Neuroscience Research, University of Texas, Southwestern Medical Center, Dallas, Texas 75235, USALynne M Bianchi - Neuroscience Program, Oberlin College, Oberlin, Ohio 44074, USAMark Henkemeyer - Center for Developmental Biology and, Kent Waldrep Foundation Center for Basic Neuroscience Research, University of Texas, Southwestern Medical Center, Dallas, Texas 75235, USABernd Fritzsch - Department of Biomedical Sciences, Creighton University, Omaha, Nebraska 68178, USA
- Resource Type
- Journal article
- Publication Details
- Neuron (Cambridge, Mass.), Vol.26(2), pp.417-430
- DOI
- 10.1016/S0896-6273(00)81174-5
- PMID
- 10839360
- NLM abbreviation
- Neuron
- ISSN
- 0896-6273
- eISSN
- 1097-4199
- Publisher
- Elsevier Inc
- Grant note
- DOI: 10.13039/100000002, name: National Institutes of Health, award: DC03121; DOI: 10.13039/100000912, name: March of Dimes Foundation; DOI: 10.13039/100000928, name: Welch Foundation; DOI: 10.13039/100005202, name: Muscular Dystrophy Association; DOI: 10.13039/501100000854, name: Human Frontier Science Program; DOI: 10.13039/100000001, name: National Science Foundation, award: 2P01 DC00215–14A1, IBN 9904566, NS36671
- Language
- English
- Date published
- 2000
- Academic Unit
- Iowa Neuroscience Institute; Biology; Craniofacial Anomalies Research Center
- Record Identifier
- 9984070733802771
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