Evidence map›Paper›PMID 29872055›Full record

ArticleNature communications2018

Variable number of TMC1-dependent mechanotransducer channels underlie tonotopic conductance gradients in the cochlea.

Maryline Beurg, Runjia Cui, Adam C Goldring, Seham Ebrahim, Robert Fettiplace, Bechara Kachar

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
7.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
  2. CaProceedings of the National Academy of Sciences of the United States of America · 2026
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  3. PIPbioRxiv : the preprint server for biology · 2026
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  9. Review
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  12. Ectopic mouse TMC1 and TMC2 alone form mechanosensitive channels that are potently modulated by TMIE.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  13. Article
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  18. Article
  19. LHFPL5 is a key element in force transmission from the tip link to the hair cell mechanotransducer channel.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  20. Article

5 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 1 country.

Maryline BeurgDepartment of Neuroscience, University of Wisconsin School of Medicine and Public Health, Madison, WI, 53706, USA.
Runjia CuiLaboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, 20892, USA.
Adam C GoldringDepartment of Neuroscience, University of Wisconsin School of Medicine and Public Health, Madison, WI, 53706, USA.
Seham EbrahimLaboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Robert FettiplaceDepartment of Neuroscience, University of Wisconsin School of Medicine and Public Health, Madison, WI, 53706, USA. fettiplace@wisc.edu.
Bechara KacharLaboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, 20892, USA. kacharb@nidcd.nih.gov.
University of Wisconsin–Madison · USNational Cancer Institute · USNational Institute on Deafness and Other Communication Disorders · USNational Institutes of Health · US

Funding

Structural and Molecular Basis of Transduction in Auditory Sensory OrgansZIADC000002 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI KACHAR, BECHARA · 2009 to 2025
$38.3M
UCD Mutant Mouse Regional Resource CenterU42OD012210 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2012 to 2026
$29.2M
INTRACELLULAR CALCIUM IN HAIR CELLSR01DC001362 · NIDCD · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT FETTIPLACE · 1992 to 2026
$11.3M
The development of mechanotransduction in cochlear hair cellsR01DC015439 · NIDCD · UNIVERSITY OF WISCONSIN-MADISON · PI FETTIPLACE, ROBERT · 2016 to 2020
$2.0M
NIDCD NIH HHS R01 DC001362NIDCD NIH HHS R01 DC015439NIH HHS U42 OD012210
6 · The paper itself

Abstract

Functional mechanoelectrical transduction (MET) channels of cochlear hair cells require the presence of transmembrane channel-like protein isoforms TMC1 or TMC2. We show that TMCs are required for normal stereociliary bundle development and distinctively influence channel properties. TMC1-dependent channels have larger single-channel conductance and in outer hair cells (OHCs) support a tonotopic apex-to-base conductance gradient. Each MET channel complex exhibits multiple conductance states in ~50 pS increments, basal MET channels having more large-conductance levels. Using mice expressing fluorescently tagged TMCs, we show a three-fold increase in number of TMC1 molecules per stereocilium tip from cochlear apex to base, mirroring the channel conductance gradient in OHCs. Single-molecule photobleaching indicates the number of TMC1 molecules per MET complex changes from ~8 at the apex to ~20 at base. The results suggest there are varying numbers of channels per MET complex, each requiring multiple TMC1 molecules, and together operating in a coordinated or cooperative manner.

Indexed as

AnimalsAnimals, NewbornCochleaHair Cells, AuditoryHair Cells, Auditory, InnerHair Cells, Auditory, OuterHair Cells, VestibularMechanotransduction, CellularMembrane ProteinsMice, KnockoutMice, TransgenicStereociliaMembrane ProteinsTMC1 protein, mouse

Identifiers

PMID29872055
PMCPMC5988745
OpenAlexW2805074423

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.