Evidence map›Paper›PMID 29233476›Full record

ArticleDevelopmental cell2017

E2F/DP Prevents Cell-Cycle Progression in Endocycling Fat Body Cells by Suppressing dATM Expression.

Ana Guarner, Robert Morris, Michael Korenjak, Myriam Boukhali, Maria Paula Zappia, Capucine Van Rechem, Johnathan R Whetstine, Sridhar Ramaswamy, Lee Zou, Maxim V Frolov and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  3. E2F regulation of theProceedings of the National Academy of Sciences of the United States of America · 2023
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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

12 authors at 3 institutions in 1 country.

Ana GuarnerMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Robert MorrisMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Michael KorenjakMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Myriam BoukhaliMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Maria Paula ZappiaDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, 900 S Ashland Avenue, Chicago, IL 60607, USA.
Capucine Van RechemMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Johnathan R WhetstineMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Sridhar RamaswamyMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Lee ZouMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Maxim V FrolovDepartment of Biochemistry and Molecular Genetics, University of Illinois at Chicago, 900 S Ashland Avenue, Chicago, IL 60607, USA.
Wilhelm HaasMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA.
Nicholas J DysonMassachusetts General Hospital Cancer Center and Harvard Medical School, Building 149 13(th) Street, Charlestown, MA 02129, USA. Electronic address: dyson@helix.mgh.harvard.edu.
Harvard University · USMassachusetts General Hospital · USUniversity of Illinois Chicago · US

Funding

Regulation of the ATR Checkpoint Kinase by DNA DamageR01GM076388 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI ZOU, LEE · 2006 to 2018
$4.3M
Understanding the Role of Histone Demethylases and Heterochromatin in Cell CycleR01GM097360 · NIGMS · RESEARCH INST OF FOX CHASE CAN CTR · PI WHETSTINE, JOHNATHAN R. · 2012 to 2020
$3.4M
Rb and Hippo tumor suppressor pathways in differentiationR01GM093827 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2011 to 2018
$2.2M
The consequences of RB-lossR01GM117413 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2016 to 2019
$2.1M
(PQC6) Molecular Determinants of Quiescent Cancer CellsR01CA185086 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI VASUDEVAN, SHOBHA · 2014 to 2017
$1.8M
Dissection and manipulation of RB functionR01CA163698 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2012 to 2016
$1.8M
Functional interaction between the mir11~998 intronic microRNA cluster and Retinoblastoma tumor suppressor pathwayR01GM110018 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2015 to 2018
$1.3M
NCI NIH HHS R01 CA163698NCI NIH HHS R01 CA185086NIGMS NIH HHS R01 GM076388NIGMS NIH HHS R01 GM093827NIGMS NIH HHS R01 GM097360NIGMS NIH HHS R01 GM110018NIGMS NIH HHS R01 GM117413
6 · The paper itself

Abstract

To understand the consequences of the complete elimination of E2F regulation, we profiled the proteome of Drosophila dDP mutants that lack functional E2F/DP complexes. The results uncovered changes in the larval fat body, a differentiated tissue that grows via endocycles. We report an unexpected mechanism of E2F/DP action that promotes quiescence in this tissue. In the fat body, dE2F/dDP limits cell-cycle progression by suppressing DNA damage responses. Loss of dDP upregulates dATM, allowing cells to sense and repair DNA damage and increasing replication of loci that are normally under-replicated in wild-type tissues. Genetic experiments show that ectopic dATM is sufficient to promote DNA synthesis in wild-type fat body cells. Strikingly, reducing dATM levels in dDP-deficient fat bodies restores cell-cycle control, improves tissue morphology, and extends animal development. These results show that, in some cellular contexts, dE2F/dDP-dependent suppression of DNA damage signaling is key for cell-cycle control and needed for normal development.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCell CycleCell Cycle ProteinsCell DivisionDNA-Binding ProteinsDNA ReplicationDrosophilaDrosophila ProteinsE2F Transcription FactorsFat BodyProtein Serine-Threonine KinasesTrans-ActivatorsTranscriptomeAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsDp transcription factor, DrosophilaDrosophila ProteinsE2F Transcription FactorsProtein Serine-Threonine KinasesTefu protein, DrosophilaTrans-ActivatorsATMDNA damageDNA replicationDPE2Fendocyclequiescencetefuunder-replication

Identifiers

PMID29233476
PMCPMC5901703
OpenAlexW2772325134

What OpenQuestion holds

Textmetadata
LicenceTDM
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.