Evidence map›Paper›PMID 21325133›Full record

ArticleGenes & development2011

Cooperation between dE2F1 and Yki/Sd defines a distinct transcriptional program necessary to bypass cell cycle exit.

Brandon N Nicolay, Battuya Bayarmagnai, Abul B M M K Islam, Nuria Lopez-Bigas, Maxim V Frolov

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. TSG-6-Mediated Extracellular Matrix Modifications Regulate Hypoxic-Ischemic Brain Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  3. Article
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  13. Article
  14. Hippo signaling is intrinsically regulated during cell cycle progression by APC/CProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  15. Review
  16. Repressive histone methylation regulates cardiac myocyte cell cycle exit.Journal of molecular and cellular cardiology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Molecular and cellular biology · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Brandon N NicolayDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois 60607, USA.
Battuya Bayarmagnai
Abul B M M K Islam
Nuria Lopez-Bigas
Maxim V Frolov
University of Illinois Chicago · USPompeu Fabra University · ES

Funding

Rb and Hippo tumor suppressor pathways in differentiationR01GM093827 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2011 to 2018
$2.2M
Characterization of novel modifiers of dE2F/RBF functionR01GM079774 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2007 to 2011
$1.3M
NIGMS NIH HHS R01 GM079774NIGMS NIH HHS R01 GM093827
6 · The paper itself

Abstract

The Hippo signaling pathway regulates organ size homeostasis, while its inactivation leads to severe hyperplasia in flies and mammals. The transcriptional coactivator Yorkie (Yki) mediates transcriptional output of the Hippo signaling. Yki lacks a DNA-binding domain and is recruited to its target promoters as a complex with DNA-binding proteins such as Scalloped (Sd). In spite of recent progress, an open question in the field is the mechanism through which the Yki/Sd transcriptional signature is defined. Here, we report that Yki/Sd synergizes with and requires the transcription factor dE2F1 to induce a specific transcriptional program necessary to bypass the cell cycle exit. We show that Yki/Sd and dE2F1 bind directly to the promoters of the Yki/Sd-dE2F1 shared target genes and activate their expression in a strong cooperative manner. Consistently, RBF, a negative regulator of dE2F1, negates this synergy and limits the overall level of expression of the Yki/Sd-dE2F1 target genes. Significantly, dE2F1 is needed for Yki/Sd-dependent full activation of these target genes, and a de2f1 mutation strongly blocks yki-induced proliferation in vivo. Thus, the Yki transcriptional program is determined through functional interactions with other transcription factors directly at target promoters. We suggest that such functional interactions would influence Yki activity and help diversify the transcriptional output of the Hippo pathway.

Indexed as

AnimalsAnimals, Genetically ModifiedCell CycleCell DivisionCell ProliferationCells, CulturedCluster AnalysisDrosophila melanogasterDrosophila ProteinsE2F1 Transcription FactorEmbryo, NonmammalianGene Expression ProfilingGene Expression Regulation, DevelopmentalMicroarray AnalysisNuclear ProteinsSignal TransductionDrosophila ProteinsE2F1 Transcription FactorNuclear Proteinssd protein, DrosophilaTrans-ActivatorsTranscription FactorsYAP-Signaling ProteinsYki protein, Drosophila

Identifiers

PMID21325133
PMCPMC3042156
OpenAlexW2023599444

What OpenQuestion holds

Textmetadata
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.