Evidence map›Paper›PMID 19336466›Full record

ArticleDevelopment (Cambridge, England)2009

Dicer-1-dependent Dacapo suppression acts downstream of Insulin receptor in regulating cell division of Drosophila germline stem cells.

Jenn-Yah Yu, Steven H Reynolds, Steve D Hatfield, Halyna R Shcherbata, Karin A Fischer, Ellen J Ward, Dang Long, Ye Ding, Hannele Ruohola-Baker

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The multifaceted roles of microRNAs in differentiation.Current opinion in cell biology · 2020
    Review
  5. Article
  6. MicroRNAs in Drosophila Cancer Models.Advances in experimental medicine and biology · 2019
    Review
  7. Article
  8. Loss ofeLife · 2017
    Article
  9. MicroRNA function in Drosophila melanogaster.Seminars in cell & developmental biology · 2017
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Receptor tyrosine kinases in Drosophila development.Cold Spring Harbor perspectives in biology · 2013
    Review
  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

9 authors at 1 institution in 1 country.

Jenn-Yah YuDepartment of Biochemistry, University of Washington, Seattle, WA 98195, USA.
Steven H Reynolds
Steve D Hatfield
Halyna R Shcherbata
Karin A Fischer
Ellen J Ward
Dang Long
Ye Ding
Hannele Ruohola-Baker
New York State Department of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is important to understand the regulation of stem cell division because defects in this process can cause altered tissue homeostasis or cancer. The cyclin-dependent kinase inhibitor Dacapo (Dap), a p21/p27 homolog, acts downstream of the microRNA (miRNA) pathway to regulate the cell cycle in Drosophila melanogaster germline stem cells (GSCs). Tissue-extrinsic signals, including insulin, also regulate cell division of GSCs. We report that intrinsic and extrinsic regulators intersect in GSC division control; the Insulin receptor (InR) pathway regulates Dap levels through miRNAs, thereby controlling GSC division. Using GFP-dap 3'UTR sensors in vivo, we show that in GSCs the dap 3'UTR is responsive to Dicer-1, an RNA endonuclease III required for miRNA processing. Furthermore, the dap 3'UTR can be directly targeted by miR-7, miR-278 and miR-309 in luciferase assays. Consistent with this, miR-278 and miR-7 mutant GSCs are partially defective in GSC division and show abnormal cell cycle marker expression, respectively. These data suggest that the GSC cell cycle is regulated via the dap 3'UTR by multiple miRNAs. Furthermore, the GFP-dap 3'UTR sensors respond to InR but not to TGF-beta signaling, suggesting that InR signaling utilizes Dap for GSC cell cycle regulation. We further demonstrate that the miRNA-based Dap regulation may act downstream of InR signaling; Dcr-1 and Dap are required for nutrition-dependent cell cycle regulation in GSCs and reduction of dap partially rescues the cell cycle defect of InR-deficient GSCs. These data suggest that miRNA- and Dap-based cell cycle regulation in GSCs can be controlled by InR signaling.

Indexed as

3' Untranslated RegionsAnimalsAnimals, Genetically ModifiedCell DivisionDrosophila melanogasterDrosophila ProteinsGene Expression RegulationGene Expression Regulation, DevelopmentalGerm CellsMicroRNAsNuclear ProteinsReceptor, InsulinRibonuclease IIIRNA HelicasesSignal TransductionStem Cells3' Untranslated Regionsdap protein, DrosophilaDcr-1 protein, DrosophilaDrosophila ProteinsMicroRNAsNuclear ProteinsReceptor, InsulinRibonuclease IIIRNA HelicasesTransforming Growth Factor beta

Identifiers

PMID19336466
PMCPMC2674257
OpenAlexW2152436544

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.