Evidence map›Paper›PMID 30531963›Full record

ArticleScientific reports2018

Xrp1 is a transcription factor required for cell competition-driven elimination of loser cells.

Ludovic Baillon, Federico Germani, Claudia Rockel, Jochen Hilchenbach, Konrad Basler

Abstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Systematic analysis of noncanonical ribosomal protein paralogs does not provide evidence for specialized functions inProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Inflammatory cytokine upd3 induces axon length-dependent synapse removal by glia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. 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

5 authors.

Ludovic BaillonInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Federico GermaniInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. federico.germani@uzh.ch.ORCID http://orcid.org/0000-0002-5604-0437
Claudia RockelInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Jochen HilchenbachInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland.
Konrad BaslerInstitute of Molecular Life Sciences, University of Zurich, Zurich, Switzerland. kb@imls.uzh.ch.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The elimination of unfit cells from a tissue is a process known in Drosophila and mammals as cell competition. In a well-studied paradigm "loser" cells that are heterozygous mutant for a haploinsufficient ribosomal protein gene are eliminated from developing tissues via apoptosis when surrounded by fitter wild-type cells, referred to as "winner" cells. However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1, which is known to help maintaining genomic stability after genotoxic stress, is necessary for the elimination of loser clones in cell competition. In loser cells, Xrp1 is transcriptionally upregulated by an autoregulatory loop and is able to trigger apoptosis - driving cell elimination. We further show that Xrp1 acts in the nucleus to regulate the transcription of several genes that have been previously involved in cell competition. We therefore speculate that Xrp1 might play a fundamental role as a molecular caretaker of the genomic integrity of tissues.

Indexed as

AnimalsApoptosisCCAAT-Enhancer-Binding ProteinsCell CommunicationDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsGene Expression RegulationRibosomesTranscriptional ActivationTranscription FactorsTranscription, GeneticUp-RegulationCCAAT-Enhancer-Binding ProteinsDNA-Binding ProteinsDrosophila ProteinsTranscription FactorsXrp1 protein, Drosophila

Identifiers

PMID30531963
PMCPMC6286310

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.