Molecular Interactions of Basic Helix Loop Helix (bHLH) Genes in Inner Ear Development
type: CreativeWork
description: The inner ear originates from an ectodermal thickening, the otic placode, which invaginates and forms the otic vesicle. The otic placode gives rise to the hearing (cochlea) and balance (vestibular) organs, comprising the sensory hair cells and sensory neurons of the cochlear (spiral) and vestibular ganglia. In mammals, inner ear sensory cells undergo terminal mitosis during embryogenesis and do not regenerate. Therefore, during postnatal life, sensory cell loss is a progressively deteriorating phenomenon leading to permanent hearing impairment. This work focuses on the molecular mechanisms regulating the cascade of events that lead to sensory cell formation during inner ear embryogenesis. Major players in these events are basic helix-loop-helix (bHLH) genes: Neurogl, Atohl and Neurodl. We investigated whether co-expression of Neurogl and Atohl in common neurosensory precursors could explain the loss of hair cells in Neurogl null mice. Analysis of terminal mitosis, using BrdU, supports previous findings regarding timing of exit from cell cycle. Specifically, we show that cell cycle exit occurs in spiral sensory neurons in a base to apex progression followed by cell cycle exit of hair cells in the organ of Corti in an apex to base progression, with some overlap of cell cycle exit in the apex for both hair cells and spiral sensory neurons. Hair cells in Neurogl null mice show cell cycle exit in an apex to base progression about 1-2 days earlier. Atohl is expressed in an apex to base progression rather then a base to apex progression as in wildtype littermates. We tested the possible expression of Atohl in neurosensory precursors using two Atohl-Cre lines. We show Atohl-Cre mediated ß-galactosidase expression in delaminating sensory neuron precursors as well as undifferentiated epithelial cells at El 1. PCR analysis shows expression of Atohl in the otocyst as early as E10.5, prior to any histology based detection techniques. Combined, these data suggest that low levels …
abstract: The inner ear originates from an ectodermal thickening, the otic placode, which invaginates and forms the otic vesicle. The otic placode gives rise to the hearing (cochlea) and balance (vestibular) organs, comprising the sensory hair cells and sensory neurons of the cochlear (spiral) and vestibular ganglia. In mammals, inner ear sensory cells undergo terminal mitosis during embryogenesis and do not regenerate. Therefore, during postnatal life, sensory cell loss is a progressively deteriorating phenomenon leading to permanent hearing impairment. This work focuses on the molecular mechanisms regulating the cascade of events that lead to sensory cell formation during inner ear embryogenesis. Major players in these events are basic helix-loop-helix (bHLH) genes: Neurogl, Atohl and Neurodl. We investigated whether co-expression of Neurogl and Atohl in common neurosensory precursors could explain the loss of hair cells in Neurogl null mice. Analysis of terminal mitosis, using BrdU, supports previous findings regarding timing of exit from cell cycle. Specifically, we show that cell cycle exit occurs in spiral sensory neurons in a base to apex progression followed by cell cycle exit of hair cells in the organ of Corti in an apex to base progression, with some overlap of cell cycle exit in the apex for both hair cells and spiral sensory neurons. Hair cells in Neurogl null mice show cell cycle exit in an apex to base progression about 1-2 days earlier. Atohl is expressed in an apex to base progression rather then a base to apex progression as in wildtype littermates. We tested the possible expression of Atohl in neurosensory precursors using two Atohl-Cre lines. We show Atohl-Cre mediated ß-galactosidase expression in delaminating sensory neuron precursors as well as undifferentiated epithelial cells at El 1. PCR analysis shows expression of Atohl in the otocyst as early as E10.5, prior to any histology based detection techniques. Combined, these data suggest that low levels …
author: Matei, Veronica Ana
language: en_US
date published: 2005-08-02
date modified: 2026-07-24T01:52:13Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/55683