Evidence map›Paper›PMID 20548101›Full record

ArticleThe Journal of cell biology2010

A robust cell cycle control mechanism limits E2F-induced proliferation of terminally differentiated cells in vivo.

Laura A Buttitta, Alexia J Katzaroff, Bruce A Edgar

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Cell cycle re-entry in the agingbioRxiv : the preprint server for biology · 2024
    Article
  4. Noncanonical function of Capicua as a growth termination signal inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Article
  6. Article
  7. Article
  8. The Krüppel-like factor Cabut has cell cycle regulatory properties similar to E2F1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Who guards the guardian? Mechanisms that restrain APC/C during the cell cycle.Biochimica et biophysica acta. Molecular cell research · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. APC/CDevelopmental cell · 2017
    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

3 authors at 2 institutions in 2 countries.

Laura A ButtittaFred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. lbuttitt@fhcrc.org
Alexia J Katzaroff
Bruce A Edgar
Fred Hutch Cancer Center · USGerman Cancer Research Center · DE

Funding

INTERDISCIPLINARY TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007183 · NICHD · UNIVERSITY OF WASHINGTON · PI RAIBLE, DAVID W · 1985 to 2015
$5.7M
Developmental control of cell cycle exitR01GM070887 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BREEDEN, LINDA L. · 2006 to 2009
$1.1M
Mechanisms controlling cell cycle exit upon terminal differentiationK99GM086517 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BUTTITTA, LAURA A · 2009 to 2010
$180k
NICHD NIH HHS T32 HD007183NICHD NIH HHS T32 HD07183NIGMS NIH HHS GM070887NIGMS NIH HHS K99 GM086517NIGMS NIH HHS R01 GM070887
6 · The paper itself

Abstract

Terminally differentiated cells in Drosophila melanogaster wings and eyes are largely resistant to proliferation upon deregulation of either E2F or cyclin E (CycE), but exogenous expression of both factors together can bypass cell cycle exit. In this study, we show this is the result of cooperation of cell cycle control mechanisms that limit E2F-CycE positive feedback and prevent cycling after terminal differentiation. Aberrant CycE activity after differentiation leads to the degradation of E2F activator complexes, which increases the proportion of CycE-resistant E2F repressor complexes, resulting in stable E2F target gene repression. If E2F-dependent repression is lost after differentiation, high anaphase-promoting complex/cyclosome (APC/C) activity degrades key E2F targets to limit cell cycle reentry. Providing both CycE and E2F activities bypasses exit by simultaneously inhibiting the APC/C and inducing a group of E2F target genes essential for cell cycle reentry after differentiation. These mechanisms are essential for proper development, as evading them leads to tissue outgrowths composed of dividing but terminally differentiated cells.

Indexed as

Cell ProliferationDrosophila melanogasterAnaphase-Promoting Complex-CyclosomeAnimalsCell CycleCell Cycle ProteinsCell DifferentiationCyclin-Dependent Kinase 2Cyclin EDrosophila ProteinsE2F Transcription FactorsGene Expression ProfilingGene Expression RegulationOligonucleotide Array Sequence AnalysisProtein Tyrosine PhosphatasesRecombinant Fusion ProteinsAnaphase-Promoting Complex-Cyclosomecdk2 protein, DrosophilaCell Cycle ProteinsCyclin-Dependent Kinase 2Cyclin EDrosophila ProteinsE2F Transcription FactorsProtein Tyrosine PhosphatasesRecombinant Fusion Proteinsstg protein, DrosophilaUbiquitin-Protein Ligase Complexes

Identifiers

PMID20548101
PMCPMC2886355
OpenAlexW2035508405

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.