Evidence map›Paper›PMID 19483676›Full record

ArticleNature2009

Genome-wide silencing in Drosophila captures conserved apoptotic effectors.

Su Kit Chew, Po Chen, Nichole Link, Kathleen A Galindo, Kristi Pogue, John M Abrams

Open access · greenAbstract read
In one paragraph

Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-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

26 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A Genetic Screen inG3 (Bethesda, Md.) · 2020
    Article
  6. Article
  7. Article
  8. Caspase-dependent non-apoptotic processes in development.Cell death and differentiation · 2017
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Mitochondrial regulation of cell death.Cold Spring Harbor perspectives in biology · 2013
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Effectors of alcohol-induced cell killing in Drosophila.Cell death and differentiation · 2012
    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

6 authors at 1 institution in 1 country.

Su Kit ChewDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.
Po Chen
Nichole Link
Kathleen A Galindo
Kristi Pogue
John M Abrams
The University of Texas Southwestern Medical Center · US

Funding

Molecular and Genetic Control of Programmed Cell DeathR01GM072124 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2004 to 2016
$4.4M
Universal Determinants of Alcohol - Induced ToxicityR01AA017328 · NIAAA · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2007 to 2010
$1.4M
Molecular and Genetic Control of Programmed Cell DeathR56GM072124 · NIGMS · UT SOUTHWESTERN MEDICAL CENTER · PI ABRAMS, JOHN M · 2008 to 2008
$353k
NIAAA NIH HHS R01 AA017328NIGMS NIH HHS R01 GM072124NIGMS NIH HHS R56 GM072124
6 · The paper itself

Abstract

Apoptosis is a conserved form of programmed cell death firmly established in the aetiology, pathogenesis and treatment of many human diseases. Central to the core machinery of apoptosis are the caspases and their proximal regulators. Current models for caspase control involve a balance of opposing elements, with variable contributions from positive and negative regulators among different cell types and species. To advance a comprehensive view of components that support caspase-dependent cell death, we conducted a genome-wide silencing screen in the Drosophila model. Our strategy used a library of double-stranded RNAs together with a chemical antagonist of Inhibitor of apoptosis proteins (IAPs) that simulates the action of native regulators in the Reaper and Smac (also known as Diablo) families. Here we present a highly validated set of targets that is necessary for death provoked by several stimuli. Among these, Tango7 is identified as a new effector. Cells depleted for this gene resisted apoptosis at a step before the induction of effector caspase activity, and the directed silencing of Tango7 in Drosophila prevented caspase-dependent programmed cell death. Unlike known apoptosis regulators in this model system, Tango7 activity did not influence stimulus-dependent loss of Drosophila DIAP1 (also known as th and IAP1), but instead regulated levels of the apical caspase Dronc (Nc). Similarly, the human Tango7 counterpart, PCID1 (also known as EIF3M), impinged on caspase 9, revealing a new regulatory axis affecting the apoptosome.

Indexed as

Gene SilencingAnimalsApoptosisApoptosomesAryl Hydrocarbon Receptor Nuclear TranslocatorCaspase 9CaspasesConserved SequenceDrosophila melanogasterDrosophila ProteinsEukaryotic Initiation Factor-3Eukaryotic Initiation FactorsGenes, InsectGenome, InsectHumansInhibitor of Apoptosis ProteinsApoptosomesAryl Hydrocarbon Receptor Nuclear TranslocatorCaspase 9CaspasesDIABLO protein, XenopusDIAP1 protein, Drosophiladronc protein, DrosophilaDrosophila ProteinseIF3m protein, DrosophilaEIF3M protein, humanEukaryotic Initiation Factor-3Eukaryotic Initiation FactorsInhibitor of Apoptosis ProteinsMitochondrial ProteinsRNA, Double-StrandedXenopus Proteins

Identifiers

PMID19483676
PMCPMC2777527
OpenAlexW2048286796

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.