GlutaredoxinV1, Main, Exploration, bibRecord, 000263

GRXCR2 Regulates Taperin Localization Critical for Stereocilia Morphology and Hearing.

Identifieur interne : 000263 ( Main/Exploration ); précédent : 000262; suivant : 000264

GRXCR2 Regulates Taperin Localization Critical for Stereocilia Morphology and Hearing.

Auteurs : Chang Liu [États-Unis] ; Na Luo [États-Unis] ; Chun-Yu Tung [États-Unis] ; Benjamin J. Perrin [États-Unis] ; Bo Zhao [États-Unis]

Source :

Cell reports [ 2211-1247 ] ; 2018.

RBID : pubmed:30380417

Descripteurs français

KwdFr :
- Animaux (MeSH), Cellules COS (MeSH), Cellules HEK293 (MeSH), Cellules ciliées auditives (métabolisme), Cellules ciliées auditives (ultrastructure), Cytosquelette d'actine (métabolisme), Cytosquelette d'actine (ultrastructure), Glutarédoxines (déficit), Glutarédoxines (métabolisme), Humains (MeSH), Liaison aux protéines (MeSH), Ouïe (MeSH), Potentiels évoqués auditifs du tronc cérébral (MeSH), Protéines (métabolisme), Souris de lignée C57BL (MeSH), Stéréocils (métabolisme), Stéréocils (ultrastructure), Surdité (anatomopathologie), Surdité (métabolisme), Surdité (physiopathologie).
MESH :
- anatomopathologie : Surdité.
- déficit : Glutarédoxines.
- métabolisme : Cellules ciliées auditives, Cytosquelette d'actine, Glutarédoxines, Protéines, Stéréocils, Surdité.
- physiopathologie : Surdité.
- ultrastructure : Animaux, Cellules COS, Cellules HEK293, Cellules ciliées auditives, Cytosquelette d'actine, Humains, Liaison aux protéines, Ouïe, Potentiels évoqués auditifs du tronc cérébral, Souris de lignée C57BL, Stéréocils.

English descriptors

KwdEn :
- Actin Cytoskeleton (metabolism), Actin Cytoskeleton (ultrastructure), Animals (MeSH), COS Cells (MeSH), Chlorocebus aethiops (MeSH), Deafness (metabolism), Deafness (pathology), Deafness (physiopathology), Evoked Potentials, Auditory, Brain Stem (MeSH), Glutaredoxins (deficiency), Glutaredoxins (metabolism), HEK293 Cells (MeSH), Hair Cells, Auditory (metabolism), Hair Cells, Auditory (ultrastructure), Hearing (MeSH), Humans (MeSH), Mice, Inbred C57BL (MeSH), Protein Binding (MeSH), Proteins (metabolism), Stereocilia (metabolism), Stereocilia (ultrastructure).
MESH :
- chemical , deficiency : Glutaredoxins.
- metabolism : Actin Cytoskeleton, Deafness, Glutaredoxins, Hair Cells, Auditory, Proteins, Stereocilia.
- pathology : Deafness.
- physiopathology : Deafness.
- ultrastructure : Actin Cytoskeleton, Hair Cells, Auditory, Stereocilia.
- Animals, COS Cells, Chlorocebus aethiops, Evoked Potentials, Auditory, Brain Stem, HEK293 Cells, Hearing, Humans, Mice, Inbred C57BL, Protein Binding.

Abstract

Mutations in human GRXCR2, which encodes a protein of undetermined function, cause hearing loss by unknown mechanisms. We found that mouse GRXCR2 localizes to the base of the stereocilia, which are actin-based mechanosensing organelles in cochlear hair cells that convert sound-induced vibrations into electrical signals. The stereocilia base also contains taperin, another protein of unknown function required for human hearing. We show that taperin and GRXCR2 form a complex and that taperin is diffused throughout the stereocilia length in Grxcr2-deficient hair cells. Stereocilia lacking GRXCR2 are longer than normal and disorganized due to the mislocalization of taperin, which could modulate the actin cytoskeleton in stereocilia. Remarkably, reducing taperin expression levels could rescue the morphological defects of stereocilia and restore the hearing of Grxcr2-deficient mice. Thus, our findings suggest that GRXCR2 is critical for the morphogenesis of stereocilia and auditory perception by restricting taperin to the stereocilia base.

DOI: 10.1016/j.celrep.2018.09.063
PubMed: 30380417
PubMed Central: PMC6317715

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000197
to stream Main, to step Curation: 000197

Le document en format XML

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<term>Actin Cytoskeleton (ultrastructure)</term>
<term>Animals (MeSH)</term>
<term>COS Cells (MeSH)</term>
<term>Chlorocebus aethiops (MeSH)</term>
<term>Deafness (metabolism)</term>
<term>Deafness (pathology)</term>
<term>Deafness (physiopathology)</term>
<term>Evoked Potentials, Auditory, Brain Stem (MeSH)</term>
<term>Glutaredoxins (deficiency)</term>
<term>Glutaredoxins (metabolism)</term>
<term>HEK293 Cells (MeSH)</term>
<term>Hair Cells, Auditory (metabolism)</term>
<term>Hair Cells, Auditory (ultrastructure)</term>
<term>Hearing (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Protein Binding (MeSH)</term>
<term>Proteins (metabolism)</term>
<term>Stereocilia (metabolism)</term>
<term>Stereocilia (ultrastructure)</term>
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<term>Cellules COS (MeSH)</term>
<term>Cellules HEK293 (MeSH)</term>
<term>Cellules ciliées auditives (métabolisme)</term>
<term>Cellules ciliées auditives (ultrastructure)</term>
<term>Cytosquelette d'actine (métabolisme)</term>
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<term>Glutarédoxines (déficit)</term>
<term>Glutarédoxines (métabolisme)</term>
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<term>Liaison aux protéines (MeSH)</term>
<term>Ouïe (MeSH)</term>
<term>Potentiels évoqués auditifs du tronc cérébral (MeSH)</term>
<term>Protéines (métabolisme)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Stéréocils (métabolisme)</term>
<term>Stéréocils (ultrastructure)</term>
<term>Surdité (anatomopathologie)</term>
<term>Surdité (métabolisme)</term>
<term>Surdité (physiopathologie)</term>
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<term>Deafness</term>
<term>Glutaredoxins</term>
<term>Hair Cells, Auditory</term>
<term>Proteins</term>
<term>Stereocilia</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules ciliées auditives</term>
<term>Cytosquelette d'actine</term>
<term>Glutarédoxines</term>
<term>Protéines</term>
<term>Stéréocils</term>
<term>Surdité</term>
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<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Deafness</term>
</keywords>
<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Actin Cytoskeleton</term>
<term>Hair Cells, Auditory</term>
<term>Stereocilia</term>
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<term>COS Cells</term>
<term>Chlorocebus aethiops</term>
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<term>HEK293 Cells</term>
<term>Hearing</term>
<term>Humans</term>
<term>Mice, Inbred C57BL</term>
<term>Protein Binding</term>
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<term>Cellules HEK293</term>
<term>Cellules ciliées auditives</term>
<term>Cytosquelette d'actine</term>
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<term>Liaison aux protéines</term>
<term>Ouïe</term>
<term>Potentiels évoqués auditifs du tronc cérébral</term>
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<front><div type="abstract" xml:lang="en">Mutations in human GRXCR2, which encodes a protein of undetermined function, cause hearing loss by unknown mechanisms. We found that mouse GRXCR2 localizes to the base of the stereocilia, which are actin-based mechanosensing organelles in cochlear hair cells that convert sound-induced vibrations into electrical signals. The stereocilia base also contains taperin, another protein of unknown function required for human hearing. We show that taperin and GRXCR2 form a complex and that taperin is diffused throughout the stereocilia length in Grxcr2-deficient hair cells. Stereocilia lacking GRXCR2 are longer than normal and disorganized due to the mislocalization of taperin, which could modulate the actin cytoskeleton in stereocilia. Remarkably, reducing taperin expression levels could rescue the morphological defects of stereocilia and restore the hearing of Grxcr2-deficient mice. Thus, our findings suggest that GRXCR2 is critical for the morphogenesis of stereocilia and auditory perception by restricting taperin to the stereocilia base.</div>
</front>
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<Abstract><AbstractText>Mutations in human GRXCR2, which encodes a protein of undetermined function, cause hearing loss by unknown mechanisms. We found that mouse GRXCR2 localizes to the base of the stereocilia, which are actin-based mechanosensing organelles in cochlear hair cells that convert sound-induced vibrations into electrical signals. The stereocilia base also contains taperin, another protein of unknown function required for human hearing. We show that taperin and GRXCR2 form a complex and that taperin is diffused throughout the stereocilia length in Grxcr2-deficient hair cells. Stereocilia lacking GRXCR2 are longer than normal and disorganized due to the mislocalization of taperin, which could modulate the actin cytoskeleton in stereocilia. Remarkably, reducing taperin expression levels could rescue the morphological defects of stereocilia and restore the hearing of Grxcr2-deficient mice. Thus, our findings suggest that GRXCR2 is critical for the morphogenesis of stereocilia and auditory perception by restricting taperin to the stereocilia base.</AbstractText>
<CopyrightInformation>Copyright © 2018 The Author(s). Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
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<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
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<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName>
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<MeshHeading><DescriptorName UI="D006309" MajorTopicYN="Y">Hearing</DescriptorName>
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<MeshHeading><DescriptorName UI="D059547" MajorTopicYN="N">Stereocilia</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
<QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName>
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</MeshHeadingList>
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GRXCR2 Regulates Taperin Localization Critical for Stereocilia Morphology and Hearing.

GRXCR2 Regulates Taperin Localization Critical for Stereocilia Morphology and Hearing.

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