Evidence map›Paper›PMID 27075174›Full record

ArticleMolecular biology of the cell2016

Different cell cycle modifications repress apoptosis at different steps independent of developmental signaling in Drosophila.

Suozhi Qi, Brian R Calvi

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. eLife · 2022
    Article
  12. Regulation and coordination of the different DNA damage responses inFrontiers in cell and developmental biology · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Molecular biology of the cell · 2019
    Article
  20. 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

2 authors.

Suozhi QiDepartment of Biology, Indiana University, Bloomington, IN 47405.
Brian R CalviDepartment of Biology, Indiana University, Bloomington, IN 47405 bcalvi@indiana.edu.

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Polypoid cell cycle regulation and genome instabilityR01GM113107 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI CALVI, BRIAN R · 2015 to 2022
$2.6M
NCATS NIH HHS UL1 TR001108NIGMS NIH HHS R01 GM113107
6 · The paper itself

Abstract

Apoptotic cell death is important for the normal development of a variety of organisms. Apoptosis is also a response to DNA damage and an important barrier to oncogenesis. The apoptotic response to DNA damage is dampened in specific cell types during development. Developmental signaling pathways can repress apoptosis, and reduced cell proliferation also correlates with a lower apoptotic response. However, because developmental signaling regulates both cell proliferation and apoptosis, the relative contribution of cell division to the apoptotic response has been hard to discern in vivo. Here we use Drosophila oogenesis as an in vivo model system to determine the extent to which cell proliferation influences the apoptotic response to DNA damage. We find that different types of cell cycle modifications are sufficient to repress the apoptotic response to ionizing radiation independent of developmental signaling. The step(s) at which the apoptosis pathway was repressed depended on the type of cell cycle modification-either upstream or downstream of expression of the p53-regulated proapoptotic genes. Our findings have important implications for understanding the coordination of cell proliferation with the apoptotic response in development and disease, including cancer and the tissue-specific responses to radiation therapy.

Indexed as

AnimalsApoptosisCDC2 Protein KinaseCell CycleCell DivisionCell ProliferationCyclin EDNA DamageDrosophila melanogasterDrosophila ProteinsOogenesisRadiation, IonizingSignal TransductionTumor Suppressor Protein p53CDC2 Protein KinaseCyclin EDrosophila ProteinsTumor Suppressor Protein p53

Identifiers

PMID27075174
PMCPMC4907722

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.