Evidence map›Paper›PMID 26958853›Full record

ArticlePloS one2016

Wound-Induced Polyploidization: Regulation by Hippo and JNK Signaling and Conservation in Mammals.

Vicki P Losick, Albert S Jun, Allan C Spradling

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-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

52 citing papers in PubMed, 76 citations in OpenAlex.

  1. Article
  2. Article
  3. Growth under pressure: The pros and cons of polyploidy induced by stress.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Review
  4. Epithelial cell fusion is required for tissue repair following UV-A irradiation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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  12. Postsynaptic BMP signaling regulates myonuclear properties inbioRxiv : the preprint server for biology · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Whole-Genome Doubling as a source of cancer: how, when, where, and why?Frontiers in cell and developmental biology · 2023
    Review
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 2 institutions in 1 country.

Vicki P LosickDepartment of Embryology, Carnegie Institution for Science, Howard Hughes Medical Institute, 3250 San Martin Dr., Baltimore, MD 21218, United States of America.
Albert S JunWilmer Eye Institute, Johns Hopkins School of Medicine, 400 N. Broadway, Baltimore, MD 21231, United States of America.
Allan C SpradlingDepartment of Embryology, Carnegie Institution for Science, Howard Hughes Medical Institute, 3250 San Martin Dr., Baltimore, MD 21218, United States of America.
Department of Embryology · USJohns Hopkins University · US

Funding

Understanding the role of thyroid hormone signaling during axolotl limb regenerationP20GM104318 · NIGMS · MOUNT DESERT ISLAND BIOLOGICAL LAB · PI DRUMMOND, IAIN A. · 2013 to 2023
$23.0M
Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
Role of unfolded protein response and COL8A2 in Fuchs corneal dystrophyR01EY019874 · NEI · JOHNS HOPKINS UNIVERSITY · PI JUN, ALBERT S · 2010 to 2014
$2.0M
Howard Hughes Medical InstituteNEI NIH HHS EY019874NEI NIH HHS R01 EY019874NIGMS NIH HHS P20 GM104318NIGMS NIH HHS R01 GM084947
6 · The paper itself

Abstract

Tissue integrity and homeostasis often rely on the proliferation of stem cells or differentiated cells to replace lost, aged, or damaged cells. Recently, we described an alternative source of cell replacement- the expansion of resident, non-dividing diploid cells by wound-induced polyploidization (WIP). Here we show that the magnitude of WIP is proportional to the extent of cell loss using a new semi-automated assay with single cell resolution. Hippo and JNK signaling regulate WIP; unexpectedly however, JNK signaling through AP-1 limits rather than stimulates the level of Yki activation and polyploidization in the Drosophila epidermis. We found that polyploidization also quantitatively compensates for cell loss in a mammalian tissue, mouse corneal endothelium, where increased cell death occurs with age in a mouse model of Fuchs Endothelial Corneal Dystrophy (FECD). Our results suggest that WIP is an evolutionarily conserved homeostatic mechanism that maintains the size and synthetic capacity of adult tissues.

Indexed as

AnimalsCorneal Dystrophies, HereditaryDisease Models, AnimalDrosophilaDrosophila ProteinsEndothelium, CornealFemaleHippo KinasesIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesMammalsMiceMice, Mutant StrainsPolyploidyProtein Serine-Threonine KinasesTranscription Factor AP-1Drosophila ProteinsHippo Kinaseshpo protein, DrosophilaIntracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesProtein Serine-Threonine KinasesTranscription Factor AP-1

Identifiers

PMID26958853
PMCPMC4784922
OpenAlexW2294184870

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.