Evidence map›Paper›PMID 26683696›Full record

ArticlePLoS genetics2015

EGFR/Ras Signaling Controls Drosophila Intestinal Stem Cell Proliferation via Capicua-Regulated Genes.

Yinhua Jin, Nati Ha, Marta Forés, Jinyi Xiang, Christine Gläßer, Julieta Maldera, Gerardo Jiménez, Bruce A Edgar

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

90 citing papers in PubMed, 144 citations in OpenAlex.

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30 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

8 authors at 4 institutions in 2 countries.

Yinhua JinDeutsches Krebsforschungszentrum (DKFZ) - Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Heidelberg, Germany.
Nati HaBiochemie-Zentrum der Universität Heidelberg (BZH), Heidelberg, Germany.
Marta ForésInstitut de Biologia Molecular de Barcelona-CSIC, Parc Científic de Barcelona, Barcelona, Spain.
Jinyi XiangDeutsches Krebsforschungszentrum (DKFZ) - Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Heidelberg, Germany.
Christine GläßerDeutsches Krebsforschungszentrum (DKFZ) - Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Heidelberg, Germany.
Julieta MalderaDeutsches Krebsforschungszentrum (DKFZ) - Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Heidelberg, Germany.
Gerardo JiménezInstitut de Biologia Molecular de Barcelona-CSIC, Parc Científic de Barcelona, Barcelona, Spain.
Bruce A EdgarDeutsches Krebsforschungszentrum (DKFZ) - Zentrum für Molekulare Biologie der Universität Heidelberg (ZMBH) Allianz, Heidelberg, Germany.
DKFZ-ZMBH Alliance · DEHeidelberg University · DEInstitut de Biologia Molecular de Barcelona · ESGerman Cancer Research Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial renewal in the Drosophila intestine is orchestrated by Intestinal Stem Cells (ISCs). Following damage or stress the intestinal epithelium produces ligands that activate the epidermal growth factor receptor (EGFR) in ISCs. This promotes their growth and division and, thereby, epithelial regeneration. Here we demonstrate that the HMG-box transcriptional repressor, Capicua (Cic), mediates these functions of EGFR signaling. Depleting Cic in ISCs activated them for division, whereas overexpressed Cic inhibited ISC proliferation and midgut regeneration. Epistasis tests showed that Cic acted as an essential downstream effector of EGFR/Ras signaling, and immunofluorescence showed that Cic's nuclear localization was regulated by EGFR signaling. ISC-specific mRNA expression profiling and DNA binding mapping using DamID indicated that Cic represses cell proliferation via direct targets including string (Cdc25), Cyclin E, and the ETS domain transcription factors Ets21C and Pointed (pnt). pnt was required for ISC over-proliferation following Cic depletion, and ectopic pnt restored ISC proliferation even in the presence of overexpressed dominant-active Cic. These studies identify Cic, Pnt, and Ets21C as critical downstream effectors of EGFR signaling in Drosophila ISCs.

Indexed as

AnimalsCell ProliferationDNA-Binding ProteinsDrosophilaDrosophila ProteinsErbB ReceptorsGene Expression Regulation, DevelopmentalHMGB ProteinsIntestinesNerve Tissue ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-etsReceptors, Invertebrate PeptideRepressor ProteinsRNA, MessengerSignal Transductioncic protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsEgfr protein, DrosophilaErbB ReceptorsEts21C protein, DrosophilaHMGB ProteinsNerve Tissue Proteinspnt protein, DrosophilaProto-Oncogene ProteinsProto-Oncogene Proteins c-etsReceptors, Invertebrate PeptideRepressor ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID26683696
PMCPMC4684324
OpenAlexW2218208207

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.