Evidence map›Paper›PMID 27737823›Full record

ArticleBiology open2016

Ecdysone signaling induces two phases of cell cycle exit in Drosophila cells.

Yongfeng Guo, Kerry Flegel, Jayashree Kumar, Daniel J McKay, Laura A Buttitta

Open access · goldAbstract read
In one paragraph

Article in Biology open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
11.0field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
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  9. Opportunistic binding of EcR to open chromatin drives tissue-specific developmental responses.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  13. Review
  14. Cellular quiescence in budding yeast.Yeast (Chichester, England) · 2021
    Review
  15. Review
  16. Article
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  19. Article
  20. Direct and widespread role for the nuclear receptor EcR in mediating the response to ecdysone inProceedings of the National Academy of Sciences of the United States of America · 2019
    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

5 authors at 2 institutions in 1 country.

Yongfeng GuoDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Kerry FlegelDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Jayashree KumarBiology Department and Genetics Department, Integrative Program for Biological and Genome Sciences, University of North Carolina, Chapel Hill, Chapel Hill, NC 27599, USA.
Daniel J McKayBiology Department and Genetics Department, Integrative Program for Biological and Genome Sciences, University of North Carolina, Chapel Hill, Chapel Hill, NC 27599, USA.
Laura A ButtittaDepartment of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA buttitta@umich.edu.ORCID http://orcid.org/0000-0002-5064-0650
University of Michigan · USUniversity of North Carolina at Chapel Hill · US

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
PREDOCTORAL TRAINING IN GENETICST32GM007544 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MORAN, JOHN V. · 1985 to 2022
$11.3M
Drosophila Transgenic RNAi Resource ProjectR01GM084947 · NIGMS · HARVARD MEDICAL SCHOOL · PI PERRIMON, NORBERT · 2008 to 2019
$9.8M
DROSOPHILA GENOMICS RESOURCE CENTERP40OD010949 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Andrew Zelhof · 2012 to 2026
$9.4M
Mechanisms controlling cell cycle exit upon terminal differentiationR00GM086517 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BUTTITTA, LAURA A · 2011 to 2013
$710k
Cell cycle re-entry in the aging adult brainR21AG047931 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BUTTITTA, LAURA A · 2015 to 2016
$416k
NIA NIH HHS R21 AG047931NIGMS NIH HHS R00 GM086517NIGMS NIH HHS R01 GM084947NIGMS NIH HHS T32 GM007544NIH HHS P40 OD010949NIH HHS P40 OD018537
6 · The paper itself

Abstract

During development, cell proliferation and differentiation must be tightly coordinated to ensure proper tissue morphogenesis. Because steroid hormones are central regulators of developmental timing, understanding the links between steroid hormone signaling and cell proliferation is crucial to understanding the molecular basis of morphogenesis. Here we examined the mechanism by which the steroid hormone ecdysone regulates the cell cycle in Drosophila We find that a cell cycle arrest induced by ecdysone in Drosophila cell culture is analogous to a G2 cell cycle arrest observed in the early pupa wing. We show that in the wing, ecdysone signaling at the larva-to-puparium transition induces Broad which in turn represses the cdc25c phosphatase String. The repression of String generates a temporary G2 arrest that synchronizes the cell cycle in the wing epithelium during early pupa wing elongation and flattening. As ecdysone levels decline after the larva-to-puparium pulse during early metamorphosis, Broad expression plummets, allowing String to become re-activated, which promotes rapid G2/M progression and a subsequent synchronized final cell cycle in the wing. In this manner, pulses of ecdysone can both synchronize the final cell cycle and promote the coordinated acquisition of terminal differentiation characteristics in the wing.

Indexed as

Cell cycleDrosophilaEcdysoneMetamorphosisSteroid hormone

Identifiers

PMID27737823
PMCPMC5155522
OpenAlexW2531945396

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.