Evidence map›Paper›PMID 26487779›Full record

ArticleDevelopment (Cambridge, England)2015

Trithorax regulates systemic signaling during Drosophila imaginal disc regeneration.

Andrea Skinner, Sumbul Jawed Khan, Rachel K Smith-Bolton

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Imaginal Disc Regeneration: Something Old, Something New.Cold Spring Harbor perspectives in biology · 2022
    Review
  6. Article
  7. The wing imaginal disc.Genetics · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Model systems for regeneration:Development (Cambridge, England) · 2020
    Review
  12. What Drosophila Can Teach Us About Radiation Biology of Human Cancers.Advances in experimental medicine and biology · 2019
    Review
  13. Review
  14. Article
  15. Imaginal disc regeneration takes flight.Current opinion in cell biology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Andrea SkinnerDepartment of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL 61853, USA.
Sumbul Jawed KhanDepartment of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL 61853, USA.
Rachel K Smith-BoltonDepartment of Cell and Developmental Biology, University of Illinois Urbana-Champaign, Urbana, IL 61853, USA rsbolton@illinois.edu.
University of Illinois Urbana-Champaign · US

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
NIGMS NIH HHS R01 GM084947NIH HHS P40 OD018537NIH HHS P40OD018537
6 · The paper itself

Abstract

Although tissue regeneration has been studied in a variety of organisms, from Hydra to humans, many of the genes that regulate the ability of each animal to regenerate remain unknown. The larval imaginal discs of the genetically tractable model organism Drosophila melanogaster have complex patterning, well-characterized development and a high regenerative capacity, and are thus an excellent model system for studying mechanisms that regulate regeneration. To identify genes that are important for wound healing and tissue repair, we have carried out a genetic screen for mutations that impair regeneration in the wing imaginal disc. Through this screen we identified the chromatin-modification gene trithorax as a key regeneration gene. Here we show that animals heterozygous for trithorax are unable to maintain activation of a developmental checkpoint that allows regeneration to occur. This defect is likely to be caused by abnormally high expression of puckered, a negative regulator of Jun N-terminal kinase (JNK) signaling, at the wound site. Insufficient JNK signaling leads to insufficient expression of an insulin-like peptide, dILP8, which is required for the developmental checkpoint. Thus, trithorax regulates regeneration signaling and capacity.

Indexed as

Gene Expression RegulationRegenerationAnimalsBody PatterningChromosomal Proteins, Non-HistoneDrosophila melanogasterDrosophila ProteinsEcdysoneEpigenesis, GeneticFemaleHeterozygoteHistonesImaginal DiscsIntercellular Signaling Peptides and ProteinsMaleMutationChromosomal Proteins, Non-HistoneDrosophila ProteinsEcdysoneHistonesinsulin-like peptide 8, DrosophilaIntercellular Signaling Peptides and ProteinsPhosphoprotein Phosphatasespuc protein, Drosophilatrx protein, DrosophilaChromatinJNK signalingRegeneration

Identifiers

PMID26487779
PMCPMC6514394
OpenAlexW1811891541

What OpenQuestion holds

Textmetadata
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.