Evidence map›Paper›PMID 31170139›Full record

ArticlePLoS biology2019

CRL4Mahj E3 ubiquitin ligase promotes neural stem cell reactivation.

Phuong Thao Ly, Ye Sing Tan, Chwee Tat Koe, Yingjie Zhang, Gengqiang Xie, Sharyn Endow, Wu-Min Deng, Fengwei Yu, Hongyan Wang

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Article
  9. A fly's eye view of quiescent neural stem cells.Oxford open neuroscience · 2022
    Review
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  13. Review
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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 6 institutions in 2 countries.

Phuong Thao LyNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-5986-2735
Ye Sing TanNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.
Chwee Tat KoeGenome Institute of Singapore, Singapore, Singapore.
Yingjie ZhangNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.
Gengqiang XieDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Sharyn EndowNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0002-0907-8889
Wu-Min DengDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States of America.
Fengwei YuNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.
Hongyan WangNeuroscience and Behavioural Disorders Programme, Duke-NUS Medical School, Singapore, Singapore.ORCID 0000-0003-4623-1878
Duke-NUS Medical School · SGFlorida State University · USDuke University · USGenome Institute of Singapore · SGNational University of Singapore · SGTemasek Life Sciences Laboratory · SG

Funding

Notch signaling and germline-soma interactions in the Drosophila ovarian modelR01GM072562 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2006 to 2025
$5.6M
Mechanistic investigation of malignant rhabdoid childhood tumor using the Drosophila modelR01CA224381 · NCI · TULANE UNIVERSITY OF LOUISIANA · PI DENG, WU-MIN · 2018 to 2022
$1.7M
NCI NIH HHS R01 CA224381NIGMS NIH HHS R01 GM072562
6 · The paper itself

Abstract

The ability of neural stem cells (NSCs) to transit between quiescence and proliferation is crucial for brain development and homeostasis. Drosophila Hippo pathway maintains NSC quiescence, but its regulation during brain development remains unknown. Here, we show that CRL4Mahj, an evolutionarily conserved E3 ubiquitin ligase, is essential for NSC reactivation (exit from quiescence). We demonstrate that damaged DNA-binding protein 1 (DDB1) and Cullin4, two core components of Cullin4-RING ligase (CRL4), are intrinsically required for NSC reactivation. We have identified a substrate receptor of CRL4, Mahjong (Mahj), which is necessary and sufficient for NSC reactivation. Moreover, we show that CRL4Mahj forms a protein complex with Warts (Wts/large tumor suppressor [Lats]), a kinase of the Hippo signaling pathway, and Mahj promotes the ubiquitination of Wts. Our genetic analyses further support the conclusion that CRL4Mahj triggers NSC reactivation by inhibition of Wts. Given that Cullin4B mutations cause mental retardation and cerebral malformation, similar regulatory mechanisms may be applied to the human brain.

Indexed as

AnimalsAnimals, Genetically ModifiedCarrier ProteinsCullin ProteinsDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsHumansNeural Stem CellsProtein BindingReceptors, Interleukin-17Signal TransductionUbiquitinationUbiquitin-Protein Ligase ComplexesUbiquitin-Protein LigasesCarrier ProteinsCul4 protein, DrosophilaCullin ProteinsDDB1 protein, humanDNA-Binding ProteinsDrosophila ProteinsIL17RB protein, humanMahj protein, DrosophilaReceptors, Interleukin-17Ubiquitin-Protein Ligase ComplexesUbiquitin-Protein Ligases

Identifiers

PMID31170139
PMCPMC6553684
OpenAlexW2948083925

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.