Evidence map›Paper›PMID 34301937›Full record

ArticleNature communications2021

YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion.

Daniel Feliciano, Carolyn M Ott, Isabel Espinosa-Medina, Aubrey V Weigel, Lorena Benedetti, Kristin M Milano, Zhonghua Tang, Tzumin Lee, Harvey J Kliman, Seth M Guller and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Cell Fusion in Reprogramming and Regeneration.Advances in experimental medicine and biology · 2026
    Review
  5. Review
  6. Biophysical Considerations in Cell Fusion.Advances in experimental medicine and biology · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Article
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

11 authors at 2 institutions in 1 country.

Daniel FelicianoJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA. felicianod@janelia.hhmi.org.ORCID http://orcid.org/0000-0003-4742-4006
Carolyn M OttJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.
Isabel Espinosa-MedinaJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.
Aubrey V WeigelJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.ORCID http://orcid.org/0000-0003-1694-4420
Lorena BenedettiJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.ORCID http://orcid.org/0000-0003-3510-0258
Kristin M MilanoDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-6897-5467
Zhonghua TangDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Tzumin LeeJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.ORCID http://orcid.org/0000-0003-0569-0111
Harvey J KlimanDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.ORCID http://orcid.org/0000-0002-2151-7071
Seth M GullerDepartment of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT, USA.
Jennifer Lippincott-SchwartzJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA. lippincottschwartzj@janelia.hhmi.org.ORCID http://orcid.org/0000-0002-8601-3501
Howard Hughes Medical Institute · USYale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR001863
6 · The paper itself

Abstract

Cells in many tissues, such as bone, muscle, and placenta, fuse into syncytia to acquire new functions and transcriptional programs. While it is known that fused cells are specialized, it is unclear whether cell-fusion itself contributes to programmatic-changes that generate the new cellular state. Here, we address this by employing a fusogen-mediated, cell-fusion system to create syncytia from undifferentiated cells. RNA-Seq analysis reveals VSV-G-induced cell fusion precedes transcriptional changes. To gain mechanistic insights, we measure the plasma membrane surface area after cell-fusion and observe it diminishes through increases in endocytosis. Consequently, glucose transporters internalize, and cytoplasmic glucose and ATP transiently decrease. This reduced energetic state activates AMPK, which inhibits YAP1, causing transcriptional-reprogramming and cell-cycle arrest. Impairing either endocytosis or AMPK activity prevents YAP1 inhibition and cell-cycle arrest after fusion. Together, these data demonstrate plasma membrane diminishment upon cell-fusion causes transient nutrient stress that may promote transcriptional-reprogramming independent from extrinsic cues.

Indexed as

Adaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnimalsBiological TransportCell FusionCell LineCell Line, TumorCell MembraneCell NucleusCells, CulturedGiant CellsHEK293 CellsHumansMembrane GlycoproteinsMiceRNA-SeqAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesG protein, vesicular stomatitis virusMembrane GlycoproteinsTranscription FactorsViral Envelope ProteinsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID34301937
PMCPMC8302681
OpenAlexW3185177784

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.