Evidence map›Paper›PMID 25119050›Full record

ArticleNature2014

Protein competition switches the function of COP9 from self-renewal to differentiation.

Lei Pan, Su Wang, Tinglin Lu, Changjiang Weng, Xiaoqing Song, Joseph K Park, Jin Sun, Zhi-Hao Yang, Junjing Yu, Hong Tang and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature, 2014. 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
4.0field-weighted citation impact, top 6% 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, 66 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  5. Article
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  10. Article
  11. Coordinating Proliferation, Polarity, and Cell Fate in theFrontiers in cell and developmental biology · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. RNA (New York, N.Y.) · 2018
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 3 countries.

Lei Pan1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China [3].
Su Wang1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA [3].
Tinglin Lu1] Center for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China [2].
Changjiang WengStowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA.
Xiaoqing SongStowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA.
Joseph K Park1] Department of Molecular Biology and Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA.
Jin SunCenter for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Zhi-Hao YangCenter for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Junjing Yu1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Chinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China.
Hong TangChinese Academy of Sciences Key Laboratory of Infection and Immunity, Institute of Biophysics, 15 Da Tun Road, Beijing 100101, China.
Dennis M McKearin1] Department of Molecular Biology and Graduate School of Biomedical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9148, USA [2] Howard Hughes Medical Institute, Chevy Chase, Maryland 20815-6789, USA.
Daniel A ChamovitzDepartment of Plant Sciences, Tel Aviv University, Tel Aviv 69978, Israel.
Jianquan NiCenter for Life Sciences, School of Medicine, Tsinghua University, Beijing 100084, China.
Ting Xie1] Stowers Institute for Medical Research, 1000 East 50th Street, Kansas City, Missouri 64110, USA [2] Department of Cell Biology and Anatomy, University of Kansas School of Medicine, 3901 Rainbow Boulevard, Kansas City, Kansas 66160, USA.
Center for Life Sciences · CNStowers Institute for Medical Research · USInstitute of Biophysics · CNThe University of Texas Southwestern Medical Center · USTel Aviv University · ILUniversity of Kansas · US

Funding

Molecular Mechanisms Regulating Drosophila Ovarian Germline Stem CellsR01GM064428 · NIGMS · STOWERS INSTITUTE FOR MEDICAL RESEARCH · PI XIE, TING · 2002 to 2010
$2.2M
Howard Hughes Medical InstituteNIGMS NIH HHS GM64428
6 · The paper itself

Abstract

The balance between stem cell self-renewal and differentiation is controlled by intrinsic factors and niche signals. In the Drosophila melanogaster ovary, some intrinsic factors promote germline stem cell (GSC) self-renewal, whereas others stimulate differentiation. However, it remains poorly understood how the balance between self-renewal and differentiation is controlled. Here we use D. melanogaster ovarian GSCs to demonstrate that the differentiation factor Bam controls the functional switch of the COP9 complex from self-renewal to differentiation via protein competition. The COP9 complex is composed of eight Csn subunits, Csn1-8, and removes Nedd8 modifications from target proteins. Genetic results indicated that the COP9 complex is required intrinsically for GSC self-renewal, whereas other Csn proteins, with the exception of Csn4, were also required for GSC progeny differentiation. Bam-mediated Csn4 sequestration from the COP9 complex via protein competition inactivated the self-renewing function of COP9 and allowed other Csn proteins to promote GSC differentiation. Therefore, this study reveals a protein-competition-based mechanism for controlling the balance between stem cell self-renewal and differentiation. Because numerous self-renewal factors are ubiquitously expressed throughout the stem cell lineage in various systems, protein competition may function as an important mechanism for controlling the self-renewal-to-differentiation switch.

Indexed as

Binding, CompetitiveCell DifferentiationAdaptor Proteins, Signal TransducingAnimalsCell ProliferationCOP9 Signalosome ComplexDNA HelicasesDrosophila melanogasterDrosophila ProteinsFemaleIntracellular Signaling Peptides and ProteinsMaleMultiprotein ComplexesNEDD8 ProteinOvaryPeptide HydrolasesAdaptor Proteins, Signal Transducingbam protein, Drosophilabgcn protein, DrosophilaCOP9 Signalosome ComplexCSN4 protein, DrosophilaCSN5 protein, DrosophilaDNA HelicasesDrosophila ProteinsIntracellular Signaling Peptides and ProteinsMultiprotein ComplexesNEDD8 ProteinNedd8 protein, DrosophilaPeptide HydrolasesUbiquitins

Identifiers

PMID25119050
OpenAlexW1981192346

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.