Evidence map›Paper›PMID 42308318›Full record

ArticleScience advances2026

Live imaging and multimodal profiling reveal transdifferentiation of a cochlear supporting cell subpopulation upon Notch inhibition.

Lama Khalaily, Shahar Kasirer, Rotem Domb, Mi Zhou, Buwei Shao, Shahar Taiber, Ran Elkon, Litao Tao, David Sprinzak, Karen B Avraham

Abstract read
In one paragraph

Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Lama KhalailyDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-1198-5242
Shahar KasirerSchool of Neurobiology, Biochemistry & Biophysics, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-4103-881X
Rotem DombDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0001-7113-2391
Mi ZhouDepartment of Biomedical Sciences, School of Medicine, Creighton University, Omaha, NE, USA.
Buwei ShaoDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0009-0001-3926-1545
Shahar TaiberDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-0787-4216
Ran ElkonDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0003-3440-1286
Litao TaoDepartment of Biomedical Sciences, School of Medicine, Creighton University, Omaha, NE, USA.ORCID 0000-0002-9801-6515
David SprinzakSchool of Neurobiology, Biochemistry & Biophysics, Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0001-6776-6957
Karen B AvrahamDepartment of Human Genetics and Computational Medicine, Gray Faculty of Medical and Health Sciences and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-4913-251X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regeneration enables organisms to repair damaged tissues, yet this capacity is notably limited in the cochlear sensory epithelium, essential for sound detection. A major cause of hearing loss arises from the irreversible loss of sensory hair cells (HCs) in the cochlea. While supporting cells (SCs) have a latent ability to transdifferentiate into HCs, this regenerative potential is rapidly lost after development. Using live imaging and single-cell multiomics of cochlear explants, we uncovered the cellular and molecular heterogeneity underlying the limited regenerative capacity of the neonatal mouse cochlea. Notch repression broadly silenced key SC genes, yet only a rare subpopulation of Deiters' cells (DC), termed transdifferentiating DCs (tDCs), initiated the transdifferentiation into HC fate. These cells underwent coordinated transcriptional and enhancer remodeling, linking epigenetic priming with morphological plasticity, while other SCs remained refractory despite robust Notch targets down-regulation. Our study provides a molecular definition of an early induced transitional DC to HC state, revealing Notch inhibition as a selective trigger that unmasks rare regenerative competence.

Indexed as

Cell TransdifferentiationCochleaLabyrinth Supporting CellsReceptors, NotchAnimalsHair Cells, AuditoryMiceRegenerationSignal TransductionReceptors, Notch

Identifiers

PMID42308318
PMCPMC13274614

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Registered trials

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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.