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Combined Atoh1 and Neurod1 Deletion Reveals Autonomous Growth of Auditory Nerve Fibers

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F86652036%3A_____%2F20%3A00541345" target="_blank" >RIV/86652036:_____/20:00541345 - isvavai.cz</a>

  • Result on the web

    <a href="https://link.springer.com/article/10.1007%2Fs12035-020-02092-0" target="_blank" >https://link.springer.com/article/10.1007%2Fs12035-020-02092-0</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s12035-020-02092-0" target="_blank" >10.1007/s12035-020-02092-0</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Combined Atoh1 and Neurod1 Deletion Reveals Autonomous Growth of Auditory Nerve Fibers

  • Original language description

    Ear development requires the transcription factors ATOH1 for hair cell differentiation and NEUROD1 for sensory neuron development. In addition, NEUROD1 negatively regulatesAtoh1gene expression. As we previously showed that deletion of theNeurod1gene in the cochlea results in axon guidance defects and excessive peripheral innervation of the sensory epithelium, we hypothesized that some of the innervation defects may be a result of abnormalities in NEUROD1 and ATOH1 interactions. To characterize the interdependency of ATOH1 and NEUROD1 in inner ear development, we generated a newAtoh1/Neurod1double null conditional deletion mutant. Through careful comparison of the effects of singleAtoh1orNeurod1gene deletion with combined doubleAtoh1andNeurod1deletion, we demonstrate that NEUROD1-ATOH1 interactions are not important for theNeurod1null innervation phenotype. We report that neurons lackingNeurod1can innervate the flat epithelium without any sensory hair cells or supporting cells left afterAtoh1deletion, indicating that neurons withNeurod1deletion do not require the presence of hair cells for axon growth. Moreover, transcriptome analysis identified genes encoding axon guidance and neurite growth molecules that are dysregulated in theNeurod1deletion mutant. Taken together, we demonstrate that much of the projections of NEUROD1-deprived inner ear sensory neurons are regulated cell-autonomously.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30103 - Neurosciences (including psychophysiology)

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2020

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Molecular Neurobiology

  • ISSN

    0893-7648

  • e-ISSN

  • Volume of the periodical

    57

  • Issue of the periodical within the volume

    12

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    16

  • Pages from-to

    5307-5323

  • UT code for WoS article

    000565831800001

  • EID of the result in the Scopus database

    2-s2.0-85090165942