Evidence map›Paper›PMID 25477468›Full record

ArticleScience (New York, N.Y.)2014

An ancient defense system eliminates unfit cells from developing tissues during cell competition.

S N Meyer, M Amoyel, C Bergantiños, C de la Cova, C Schertel, K Basler, L A Johnston

Open access · greenAbstract read
In one paragraph

Article in Science (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.

0numbers the graph read from it
0cells of the map it votes in
127citing 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

127 citing papers in PubMed, 262 citations in OpenAlex.

  1. Article
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  11. Journal of virology · 2025
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  18. Functions ofFrontiers in cell and developmental biology · 2025
    Review
  19. Article
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67 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 2 countries.

S N MeyerInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
M AmoyelDepartment of Genetics and Development, Columbia University, New York, NY 10032, USA.
C BergantiñosDepartment of Genetics and Development, Columbia University, New York, NY 10032, USA.
C de la CovaDepartment of Genetics and Development, Columbia University, New York, NY 10032, USA.
C SchertelInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
K BaslerInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. konrad.basler@imls.uzh.ch lj180@columbia.edu.
L A JohnstonDepartment of Genetics and Development, Columbia University, New York, NY 10032, USA. konrad.basler@imls.uzh.ch lj180@columbia.edu.
Columbia University · USUniversity of Zurich · CH

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
Mechanisms of cell competition that regulate growth during developmentR01GM078464 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI JOHNSTON, LAURA A · 2006 to 2018
$3.8M
A novel signaling pathway for tissue homeostasisR21HD067918 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI JOHNSTON, LAURA A · 2011 to 2012
$443k
NICHD NIH HHS R21 HD067918NIGMS NIH HHS R01 GM078464NIGMS NIH HHS R01 GM084947NIGMS NIH HHS R01-GM084947NIH HHS P40 OD018537NIH HHS P40OD018537
6 · The paper itself

Abstract

Developing tissues that contain mutant or compromised cells present risks to animal health. Accordingly, the appearance of a population of suboptimal cells in a tissue elicits cellular interactions that prevent their contribution to the adult. Here we report that this quality control process, cell competition, uses specific components of the evolutionarily ancient and conserved innate immune system to eliminate Drosophila cells perceived as unfit. We find that Toll-related receptors (TRRs) and the cytokine Spätzle (Spz) lead to NFκB-dependent apoptosis. Diverse "loser" cells require different TRRs and NFκB factors and activate distinct pro-death genes, implying that the particular response is stipulated by the competitive context. Our findings demonstrate a functional repurposing of components of TRRs and NFκB signaling modules in the surveillance of cell fitness during development.

Indexed as

AnimalsApoptosisCell CommunicationDrosophila melanogasterDrosophila ProteinsImmunity, InnateMutationNeuropeptidesNF-kappa BToll-Like ReceptorsTranscription FactorsTranscription, GeneticDrosophila ProteinsHID protein, DrosophilaNeuropeptidesNF-kappa BRel protein, Drosophilaspz protein, DrosophilaToll-Like ReceptorsTranscription Factors

Identifiers

PMID25477468
PMCPMC5095928
OpenAlexW2043888953

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.