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Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation.

Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Research Abstract Details 

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  • Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Abstract Text:

    The proneuronal gene neurogenin 1 (ngn1) is essential for development of the inner-ear sensory neurons that are completely absent in ngn1 null mutants. Neither afferent, efferent, nor autonomic nerve fibers were detected in the ears of ngn1 null mutants. We suggest that efferent and autonomic fibers are lost secondarily to the absence of afferents. In this article we show that ngn1 null mutants develop smaller sensory epithelia with morphologically normal hair cells. In particular, the saccule is reduced dramatically and forms only a small recess with few hair cells along a duct connecting the utricle with the cochlea. Hair cells of newborn ngn1 null mutants show no structural abnormalities, suggesting that embryonic development of hair cells is independent of innervation. However, the less regular pattern of dispersal within sensory epithelia may be caused by some effects of afferents or to the stunted growth of the sensory epithelia. Tracing of facial and stato-acoustic nerves in control and ngn1 null mutants showed that only the distal, epibranchial, placode-derived sensory neurons of the geniculate ganglion exist in mutants. Tracing further showed that these geniculate ganglion neurons project exclusively to the solitary tract. In addition to the normal complement of facial branchial and visceral motoneurons, ngnl null mutants have some trigeminal motoneurons and contralateral inner-ear efferents projecting, at least temporarily, through the facial nerve. These data suggest that some neurons in the brainstem (e.g., inner-ear efferents, trigeminal motoneurons) require afferents to grow along and redirect to ectopic cranial nerve roots in the absence of their corresponding sensory roots.

    Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Publishing Authors By Initials

    For similar proteins: transcription factors research abstracts see: proteins: transcription factors research

    PUBMED ID PMID:

    MEDLINE DATE:

    Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Journal Published:

    PUBLICATION TYPE: Research Support, U.S. Gov't,

    Journal: Journal of the Association for Research in Otolary

    VOLUME: 1

    Page Numbers: 129-43

    Journal Abbreviation: J. Assoc. Res. Otolaryngol.

    ISSN: 1525-3961

    DAY: 17

    MONTH: Sep

    YEAR: 2000

    Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100892857

    Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Keywords Mesh Terms:

    KEYWORDS: Transcription Factors

    MESH TERMS: pathology

    Chemical & Substance for Abstract: Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation. Information

    Substance Name: Neurog1 protein, mouse

    Registry Number: 182238-50-2

    Grant and Affiliation Information for Neurogenin 1 null mutant ears develop fewer, morphologically normal hair cells in smaller sensory epithelia devoid of innervation.

    AFFILIATION: Dana Farber Cancer Institute, Boston, MA 02115, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIDCD

    GRANT: 2P01 DC00215-14A1

    ACRONYM: DC

    MEDLINETA: J Assoc Res Otolaryngol

    REFSOURCE: J Assoc Res Otolaryngol 2000 Dec;1(4):32

    DATABASENAME:

    ACCESSION NUMBER:

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