Evidence map›Paper›PMID 19546319›Full record

ArticleGenetics2009

Mosaic genetic screen for suppressors of the de2f1 mutant phenotype in Drosophila.

Aaron M Ambrus, Vanya I Rasheva, Brandon N Nicolay, Maxim V Frolov

Open access · bronzeAbstract readEvaluation Study
In one paragraph

Article in Genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. GFZF, a GlutathioneMolecular and cellular biology · 2018
    Article
  5. AnOpen biology · 2017
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 1 institution in 1 country.

Aaron M AmbrusDepartment of Biochemistry and Molecular Genetics, University of Illinois, Chicago, Illinois 60607, USA.
Vanya I Rasheva
Brandon N Nicolay
Maxim V Frolov
University of Illinois Chicago · US

Funding

Characterization of novel modifiers of dE2F/RBF functionR01GM079774 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FROLOV, MAXIM · 2007 to 2011
$1.3M
Genetic Interaction Between the pRB and Warts Tumor Suppressor PathwaysF31AG032169 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NICOLAY, BRANDON · 2008 to 2010
$99k
NIA NIH HHS F31 AG032169NIGMS NIH HHS GM079774NIGMS NIH HHS R01 GM079774
6 · The paper itself

Abstract

The growth suppressive function of the retinoblastoma (pRB) tumor suppressor family is largely attributed to its ability to negatively regulate the family of E2F transcriptional factors and, as a result, to repress E2F-dependent transcription. Deregulation of the pRB pathway is thought to be an obligatory event in most types of cancers. The large number of mammalian E2F proteins is one of the major obstacles that complicate their genetic analysis. In Drosophila, the E2F family consists of only two members. They are classified as an activator (dE2F1) and a repressor (dE2F2). It has been previously shown that proliferation of de2f1 mutant cells is severely reduced due to unchecked activity of the repressor dE2F2 in these cells. We report here a mosaic screen utilizing the de2f1 mutant phenotype to identify suppressors that overcome the dE2F2/RBF-dependent proliferation block. We have isolated l(3)mbt and B52, which are known to be required for dE2F2 function, as well as genes that were not previously linked to the E2F/pRB pathway such as Doa, gfzf, and CG31133. Inactivation of gfzf, Doa, or CG31133 does not relieve repression by dE2F2. We have shown that gfzf and CG31133 potentiate E2F-dependent activation and synergize with inactivation of RBF, suggesting that they may act in parallel to dE2F. Thus, our results demonstrate the efficacy of the described screening strategy for studying regulation of the dE2F/RBF pathway in vivo.

Indexed as

Suppression, GeneticAlgorithmsAnimalsAnimals, Genetically ModifiedCell ProliferationCells, CulturedDrosophila melanogasterDrosophila ProteinsFemaleGenetic Complementation TestGenetic TestingMaleModels, GeneticMosaicismMutant ProteinsPhenotypeDrosophila ProteinsE2f1 protein, DrosophilaMutant ProteinsRbf protein, DrosophilaRetinoblastoma ProteinTranscription Factors

Identifiers

PMID19546319
PMCPMC2746169
OpenAlexW2111307513

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.