Evidence map›Paper›PMID 24931167›Full record

ArticleOncogene2015

An intergenic regulatory region mediates Drosophila Myc-induced apoptosis and blocks tissue hyperplasia.

C Zhang, S Casas-Tintó, G Li, N Lin, M Chung, E Moreno, K H Moberg, L Zhou

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021
    Review
  4. Dronc-independent basal executioner caspase activity sustainsProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  5. Article
  6. TheG3 (Bethesda, Md.) · 2018
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

C Zhang1] Department of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA [2] Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.
S Casas-TintóCajal Institute, Spanish Research Council (CSIC), Madrid, Spain.
G Li1] Department of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA [2] UF Genetics Institute, University of Florida, Gainesville, FL, USA.
N LinDepartment of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA.
M ChungDepartment of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA.
E MorenoMolecular Oncology Program, Spanish National Cancer Centre (CNIO), Madrid, Spain.
K H MobergDepartment of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.
L Zhou1] Department of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA [2] UF Genetics Institute, University of Florida, Gainesville, FL, USA.
University of Florida Health · USEmory University · USInstituto Cajal · ESSpanish National Cancer Research Centre · ESUniversity of Florida · US

Funding

Probing Complexity of UV Induced Apoptosis in DrosophilaR01CA095542 · NCI · UNIVERSITY OF FLORIDA · PI ZHOU, LEI · 2003 to 2007
$1.2M
Rapid Induction of apoptosis against viral infectionR01GM106174 · NIGMS · UNIVERSITY OF FLORIDA · PI ZHOU, LEI · 2014 to 2017
$1.1M
NCI NIH HHS R01 CA095542NIGMS NIH HHS R01 GM106174
6 · The paper itself

Abstract

Induction of cell-autonomous apoptosis following oncogene-induced overproliferation is a major tumor-suppressive mechanism in vertebrates. However, the detailed mechanism mediating this process remains enigmatic. In this study, we demonstrate that dMyc-induced cell-autonomous apoptosis in the fruit fly Drosophila melanogaster relies on an intergenic sequence termed the IRER (irradiation-responsive enhancer region). The IRER mediates the expression of surrounding proapoptotic genes, and we use an in vivo reporter of the IRER chromatin state to gather evidence that epigenetic control of DNA accessibility within the IRER is an important determinant of the strength of this response to excess dMyc. In a previous work, we showed that the IRER also mediates P53-dependent induction of proapoptotic genes following DNA damage, and the chromatin conformation within IRER is regulated by polycomb group-mediated histone modifications. dMyc-induced apoptosis and the P53-mediated DNA damage response thus overlap in a requirement for the IRER. The epigenetic mechanisms controlling IRER accessibility appear to set thresholds for the P53- and dMyc-induced expression of apoptotic genes in vivo and may have a profound impact on cellular sensitivity to oncogene-induced stress.

Indexed as

Regulatory Sequences, Nucleic AcidAnimalsApoptosisChromatinDNA-Binding ProteinsDNA DamageDrosophila melanogasterDrosophila ProteinsEpigenesis, GeneticGenome, InsectHyperplasiaTranscription FactorsTumor Suppressor Protein p53Wings, AnimalChromatinDNA-Binding ProteinsDrosophila ProteinsMyc protein, Drosophilap53 protein, DrosophilaTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID24931167
PMCPMC4268096
OpenAlexW2017476823

What OpenQuestion holds

Textmetadata
LicenceTDM
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.