Evidence map›Paper›PMID 28239148›Full record

ArticleNature communications2017

Amotl1 mediates sequestration of the Hippo effector Yap1 downstream of Fat4 to restrict heart growth.

Chiara V Ragni, Nicolas Diguet, Jean-François Le Garrec, Marta Novotova, Tatiana P Resende, Sorin Pop, Nicolas Charon, Laurent Guillemot, Lisa Kitasato, Caroline Badouel and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

62 citing papers in PubMed, 110 citations in OpenAlex.

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  13. Role of angiomotin family members in human diseases (Review).Experimental and therapeutic medicine · 2024
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2 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

15 authors at 7 institutions in 4 countries.

Chiara V RagniInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Nicolas DiguetInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Jean-François Le GarrecInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Marta NovotovaInstitute of Molecular Physiology and Genetics, Centre of Biosciences, Slovak Academy of Sciences, Dúbravská cesta 9, 84005 Bratislava, Slovak Republic.
Tatiana P ResendeInstituto de Investigação e Inovação em Saúde (i3S), Universidade do Porto, 4200-135 Porto, Portugal.ORCID 0000-0002-1116-5770
Sorin PopInstitut Pasteur, Quantitative Image Analysis Unit, 75015 Paris, France.
Nicolas CharonENS Cachan, Center of Mathematics and Their Applications, 94235 Cachan, France.
Laurent GuillemotInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Lisa KitasatoInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Caroline BadouelSamuel Lunenfeld Research Institute, Mt Sinai Hospital, Toronto, Ontario, Canada M5G 1X5.
Alexandre DufourInstitut Pasteur, Quantitative Image Analysis Unit, 75015 Paris, France.ORCID 0000-0002-9417-7389
Jean-Christophe Olivo-MarinInstitut Pasteur, Quantitative Image Analysis Unit, 75015 Paris, France.
Alain TrouvéENS Cachan, Center of Mathematics and Their Applications, 94235 Cachan, France.
Helen McNeillSamuel Lunenfeld Research Institute, Mt Sinai Hospital, Toronto, Ontario, Canada M5G 1X5.
Sigolène M MeilhacInstitut Pasteur, Department of Developmental and Stem Cell Biology, 75015 Paris, France.
Centre National de la Recherche Scientifique · FRÉcole Normale Supérieure Paris-Saclay · FRMount Sinai Hospital · CAInserm · FRInstitut Pasteur · FRSlovak Academy of Sciences · SKUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although in flies the atypical cadherin Fat is an upstream regulator of Hippo signalling, the closest mammalian homologue, Fat4, has been shown to regulate tissue polarity rather than growth. Here we show in the mouse heart that Fat4 modulates Hippo signalling to restrict growth. Fat4 mutant myocardium is thicker, with increased cardiomyocyte size and proliferation, and this is mediated by an upregulation of the transcriptional activity of Yap1, an effector of the Hippo pathway. Fat4 is not required for the canonical activation of Hippo kinases but it sequesters a partner of Yap1, Amotl1, out of the nucleus. The nuclear translocation of Amotl1 is accompanied by Yap1 to promote cardiomyocyte proliferation. We, therefore, identify Amotl1, which is not present in flies, as a mammalian intermediate for non-canonical Hippo signalling, downstream of Fat4. This work uncovers a mechanism for the restriction of heart growth at birth, a process which impedes the regenerative potential of the mammalian heart.

Indexed as

Adaptor Proteins, Signal TransducingAngiopoietin-Like Protein 1AnimalsAnimals, NewbornCadherinsCardiomegalyCell Cycle ProteinsCell ProliferationDesmosomesGene Expression Regulation, DevelopmentalHeartMembrane ProteinsMiceModels, BiologicalPhosphoproteinsProtein BindingAdaptor Proteins, Signal TransducingAmotl1 protein, mouseAngiopoietin-Like Protein 1CadherinsCell Cycle ProteinsFat4 protein, mouseMembrane ProteinsPhosphoproteinsYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID28239148
PMCPMC5333361
OpenAlexW2594062767

What OpenQuestion holds

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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.