Evidence map›Paper›PMID 22140578›Full record

ArticlePloS one2011

Hole-in-one mutant phenotypes link EGFR/ERK signaling to epithelial tissue repair in Drosophila.

Jennifer A Geiger, Lara Carvalho, Isabel Campos, Ana Catarina Santos, Antonio Jacinto

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  6. Transposable elements contribute to the genomic response to insecticides inPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
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  7. Review
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  11. Damage signals in the insect immune response.Frontiers in plant science · 2014
    Review
  12. Article
  13. Review
  14. Article
  15. 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 at 1 institution in 1 country.

Jennifer A GeigerTissue Morphogenesis and Repair Unit, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal.
Lara Carvalho
Isabel Campos
Ana Catarina Santos
Antonio Jacinto
University of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpithelia act as physical barriers protecting living organisms and their organs from the surrounding environment. Simple epithelial tissues have the capacity to efficiently repair wounds through a resealing mechanism. The known molecular mechanisms underlying this process appear to be conserved in both vertebrates and invertebrates, namely the involvement of the transcription factors Grainy head (Grh) and Fos. In Drosophila, Grh and Fos lead to the activation of wound response genes required for epithelial repair. ERK is upstream of this pathway and known to be one of the first kinases to be activated upon wounding. However, it is still unclear how ERK activation contributes to a proper wound response and which molecular mechanisms regulate its activation. METHODOLOGY/PRINCIPAL

findingsIn a previous screen, we isolated mutants with defects in wound healing. Here, we describe the role of one of these genes, hole-in-one (holn1), in the wound healing process. Holn1 is a GYF domain containing protein that we found to be required for the activation of several Grh and Fos regulated wound response genes at the wound site. We also provide evidence suggesting that Holn1 may be involved in the Ras/ERK signaling pathway, by acting downstream of ERK. Finally, we show that wound healing requires the function of EGFR and ERK signaling. CONCLUSIONS/SIGNIFICANCE: Based on these data, we conclude that holn1 is a novel gene required for a proper wound healing response. We further propose and discuss a model whereby Holn1 acts downstream of EGFR and ERK signaling in the Grh/Fos mediated wound closure pathway.

Indexed as

Wound HealingActomyosinAllelesAnimalsCell NucleusDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianEnzyme ActivationEpitheliumErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Expression RegulationGene Knockdown TechniquesGenes, ReporterMAP Kinase Signaling SystemActomyosinDrosophila ProteinsErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHoln1 protein, DrosophilaNuclear Proteinsras ProteinsRNA, Messenger

Identifiers

PMID22140578
PMCPMC3226689
OpenAlexW2076853957

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.