Evidence map›Paper›PMID 37378613›Full record

ArticleThe Journal of cell biology2023

Mechanical control of the mammalian circadian clock via YAP/TAZ and TEAD.

Juan F Abenza, Leone Rossetti, Malèke Mouelhi, Javier Burgués, Ion Andreu, Keith Kennedy, Pere Roca-Cusachs, Santiago Marco, Jordi García-Ojalvo, Xavier Trepat

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

19 citing papers in PubMed, 20 citations in OpenAlex.

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  13. Circadian clock communication during homeostasis and ageing.Nature reviews. Molecular cell biology · 2025
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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 at 4 institutions in 1 country.

Juan F Abenza *Institute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0003-1685-1013
Leone Rossetti *Institute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0002-4667-9640
Malèke MouelhiInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0002-1813-6526
Javier BurguésInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0002-7327-6396
Ion AndreuInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0002-8374-152X
Keith KennedyDepartment of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain.ORCID 0000-0001-5551-7304
Pere Roca-CusachsInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0001-6947-961X
Santiago MarcoInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0003-2663-2965
Jordi García-OjalvoDepartment of Experimental and Health Sciences, Universitat Pompeu Fabra, Barcelona, Spain.ORCID 0000-0002-3716-7520
Xavier TrepatInstitute for Bioengineering of Catalonia , The Barcelona Institute for Science and Technology , Barcelona, Spain.ORCID 0000-0002-7621-5214
Barcelona Institute of Science and Technology · ESUniversitat Pompeu Fabra · ESBiomedical Research Networking Center in Bioengineering, Biomaterials and Nanomedicine · ESInstitució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autonomous circadian clocks exist in nearly every mammalian cell type. These cellular clocks are subjected to a multilayered regulation sensitive to the mechanochemical cell microenvironment. Whereas the biochemical signaling that controls the cellular circadian clock is increasingly well understood, mechanisms underlying regulation by mechanical cues are largely unknown. Here we show that the fibroblast circadian clock is mechanically regulated through YAP/TAZ nuclear levels. We use high-throughput analysis of single-cell circadian rhythms and apply controlled mechanical, biochemical, and genetic perturbations to study the expression of the clock gene Rev-erbα. We observe that Rev-erbα circadian oscillations are disrupted with YAP/TAZ nuclear translocation. By targeted mutations and overexpression of YAP/TAZ, we show that this mechanobiological regulation, which also impacts core components of the clock such as Bmal1 and Cry1, depends on the binding of YAP/TAZ to the transcriptional effector TEAD. This mechanism could explain the impairment of circadian rhythms observed when YAP/TAZ activity is upregulated, as in cancer and aging.

Indexed as

Circadian ClocksTEA Domain Transcription FactorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsYAP-Signaling ProteinsAnimalsCircadian RhythmMammalsSignal TransductionTEA Domain Transcription FactorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsYAP-Signaling Proteins

Identifiers

PMID37378613
PMCPMC10308087
OpenAlexW4382344396

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.