Evidence map›Paper›PMID 22242003›Full record

ArticlePLoS genetics2011

Duox, Flotillin-2, and Src42A are required to activate or delimit the spread of the transcriptional response to epidermal wounds in Drosophila.

Michelle T Juarez, Rachel A Patterson, Efren Sandoval-Guillen, William McGinnis

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Parallel repair mechanisms in plants and animals.Disease models & mechanisms · 2023
    Article
  5. Wound Healing Insights from Flies and Fish.Cold Spring Harbor perspectives in biology · 2022
    Review
  6. Article
  7. Injury-induced inflammatory signaling and hematopoiesis inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Grainyhead-like (Grhl) Target Genes in Development and Cancer.International journal of molecular sciences · 2022
    Review
  9. DUOX1 in mammalian disease pathophysiology.Journal of molecular medicine (Berlin, Germany) · 2021
    Review
  10. Article
  11. Acute exposure of Nicotine duringmicroPublication biology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Translating Research as an Approach to Enhance Science Engagement.International journal of environmental research and public health · 2018
    Article
  16. Review
  17. DUOX1 Silencing in Mammary Cell Alters the Response to Genotoxic Stress.Oxidative medicine and cellular longevity · 2018
    Article
  18. Article
  19. Article
  20. Toll pathway is required for wound-induced expression of barrier repair genes in theProceedings of the National Academy of Sciences of the United States of America · 2017
    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

4 authors at 1 institution in 1 country.

Michelle T JuarezSection of Cell and Developmental Biology, Division of Biology, University of California San Diego, La Jolla, California, United States of America.
Rachel A Patterson
Efren Sandoval-Guillen
William McGinnis
University of California, San Diego · US

Funding

UCSD/SDSU IRACDAK12GM068524 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TREJO, JOANN · 2003 to 2025
$24.4M
Specificity in Homeotic Response ElementsR37HD028315 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCGINNIS, WILLIAM JAMES · 2006 to 2015
$2.9M
Regulation of epidermal barrier wound repairR01GM077197 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCGINNIS, WILLIAM JAMES · 2007 to 2010
$998k
NICHD NIH HHS R37 HD028315NIGMS NIH HHS K12 GM068524NIGMS NIH HHS K12 GM68524NIGMS NIH HHS R01 GM077197
6 · The paper itself

Abstract

The epidermis is the largest organ of the body for most animals, and the first line of defense against invading pathogens. A breach in the epidermal cell layer triggers a variety of localized responses that in favorable circumstances result in the repair of the wound. Many cellular and genetic responses must be limited to epidermal cells that are close to wounds, but how this is regulated is still poorly understood. The order and hierarchy of epidermal wound signaling factors are also still obscure. The Drosophila embryonic epidermis provides an excellent system to study genes that regulate wound healing processes. We have developed a variety of fluorescent reporters that provide a visible readout of wound-dependent transcriptional activation near epidermal wound sites. A large screen for mutants that alter the activity of these wound reporters has identified seven new genes required to activate or delimit wound-induced transcriptional responses to a narrow zone of cells surrounding wound sites. Among the genes required to delimit the spread of wound responses are Drosophila Flotillin-2 and Src42A, both of which are transcriptionally activated around wound sites. Flotillin-2 and constitutively active Src42A are also sufficient, when overexpressed at high levels, to inhibit wound-induced transcription in epidermal cells. One gene required to activate epidermal wound reporters encodes Dual oxidase, an enzyme that produces hydrogen peroxide. We also find that four biochemical treatments (a serine protease, a Src kinase inhibitor, methyl-ß-cyclodextrin, and hydrogen peroxide) are sufficient to globally activate epidermal wound response genes in Drosophila embryos. We explore the epistatic relationships among the factors that induce or delimit the spread of epidermal wound signals. Our results define new genetic functions that interact to instruct only a limited number of cells around puncture wounds to mount a transcriptional response, mediating local repair and regeneration.

Indexed as

Animalsbeta-CyclodextrinsDrosophila melanogasterDrosophila ProteinsEpidermisGene Expression RegulationHydrogen PeroxideMembrane ProteinsMutationNADPH OxidasesProto-Oncogene Proteins pp60(c-src)Signal TransductionTranscription FactorsWound Healingbeta-CyclodextrinsDrosophila Proteinsdual oxidase, DrosophilaflotillinsHydrogen PeroxideMembrane Proteinsmethyl-beta-cyclodextrinNADPH OxidasesProto-Oncogene Proteins pp60(c-src)Src42A protein, DrosophilaTranscription Factors

Identifiers

PMID22242003
PMCPMC3248467
OpenAlexW2059511014

What OpenQuestion holds

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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.