Evidence map›Paper›PMID 18688282›Full record

ArticlePLoS genetics2008

E2F and p53 induce apoptosis independently during Drosophila development but intersect in the context of DNA damage.

Nam-Sung Moon, Luisa Di Stefano, Erick J Morris, Reena Patel, Kristin White, Nicholas J Dyson

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 66 citations in OpenAlex.

  1. Plastic Fly: WhatInternational journal of molecular sciences · 2024
    Article
  2. Article
  3. Article
  4. International journal of molecular sciences · 2023
    Article
  5. Article
  6. Regulation and coordination of the different DNA damage responses inFrontiers in cell and developmental biology · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Molecular biology of the cell · 2019
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Nam-Sung MoonMassachusetts General Hospital Cancer Research Center, Charlestown, Massachusetts, United States of America.
Luisa Di Stefano
Erick J Morris
Reena Patel
Kristin White
Nicholas J Dyson
Massachusetts General Hospital · USHarvard University · USCancer Research Center · US

Funding

The E2F/RBF networkR01GM053203 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 1995 to 2010
$4.2M
APOPTOSIS IN DROSOPHILA--FROM REAPER TO DEATHR01GM055568 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI WHITE, KRISTIN · 1997 to 2011
$3.8M
The Enhancement and Suppression of E2F-Dependent ApoptosisR01GM081607 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2008 to 2011
$1.3M
NIGMS NIH HHS GM53203NIGMS NIH HHS GM55568NIGMS NIH HHS GM81607NIGMS NIH HHS R01 GM053203NIGMS NIH HHS R01 GM055568NIGMS NIH HHS R01 GM081607
6 · The paper itself

Abstract

In mammalian cells, RB/E2F and p53 are intimately connected, and crosstalk between these pathways is critical for the induction of cell cycle arrest or cell death in response to cellular stresses. Here we have investigated the genetic interactions between RBF/E2F and p53 pathways during Drosophila development. Unexpectedly, we find that the pro-apoptotic activities of E2F and p53 are independent of one another when examined in the context of Drosophila development: apoptosis induced by the deregulation of dE2F1, or by the overexpression of dE2F1, is unaffected by the elimination of dp53; conversely, dp53-induced phenotypes are unaffected by the elimination of dE2F activity. However, dE2F and dp53 converge in the context of a DNA damage response. Both dE2F1/dDP and dp53 are required for DNA damage-induced cell death, and the analysis of rbf1 mutant eye discs indicates that dE2F1/dDP and dp53 cooperatively promote cell death in irradiated discs. In this context, the further deregulation in the expression of pro-apoptotic genes generates an additional sensitivity to apoptosis that requires both dE2F/dDP and dp53 activity. This sensitivity differs from DNA damage-induced apoptosis in wild-type discs (and from dE2F/dDP-induced apoptosis in un-irradiated rbf1 mutant eye discs) by being dependent on both hid and reaper. These results show that pro-apoptotic activities of dE2F1 and dp53 are surprisingly separable: dp53 is required for dE2F-dependent apoptosis in the response to DNA damage, but it is not required for dE2F-dependent apoptosis caused simply by the inactivation of rbf1.

Indexed as

ApoptosisDNA DamageGene Expression Regulation, DevelopmentalAnimalsDrosophilaDrosophila ProteinsE2F Transcription FactorsFemaleMaleRetinoblastoma ProteinSignal TransductionTranscription FactorsTumor Suppressor Protein p53Drosophila ProteinsE2f1 protein, DrosophilaE2F Transcription Factorsp53 protein, DrosophilaRbf protein, DrosophilaRetinoblastoma ProteinTranscription FactorsTumor Suppressor Protein p53

Identifiers

PMID18688282
PMCPMC2491587
OpenAlexW2168156118

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.