Evidence map›Paper›PMID 30470739›Full record

ArticleNature communications2018

Topoisomerase 3β interacts with RNAi machinery to promote heterochromatin formation and transcriptional silencing in Drosophila.

Seung Kyu Lee, Yutong Xue, Weiping Shen, Yongqing Zhang, Yuyoung Joo, Muzammil Ahmad, Madoka Chinen, Yi Ding, Wai Lim Ku, Supriyo De and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. 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
1.2field-weighted citation impact, top 21% 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, 38 citations in OpenAlex.

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  17. Nuclear architecture and the structural basis of mitotic memory.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Review
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  19. 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

17 authors at 2 institutions in 1 country.

Seung Kyu LeeLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Yutong XueLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Weiping ShenLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Yongqing ZhangLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Yuyoung JooLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Muzammil AhmadLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Madoka ChinenLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive Kidney Diseases, Bethesda, MD, 20892, USA.
Yi DingSystem Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Wai Lim KuSystem Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0002-8859-6771
Supriyo DeLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Elin LehrmannLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.ORCID http://orcid.org/0000-0002-9869-9475
Kevin G BeckerLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Elissa P LeiLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive Kidney Diseases, Bethesda, MD, 20892, USA.
Keji ZhaoSystem Biology Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0001-5559-6233
Sige ZouTranslational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Alexei SharovLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Weidong WangLab of Genetics and Genomics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA. wangw@grc.nia.nih.gov.
National Institutes of Health · USNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Chromatin Insulator Function and Nuclear OrganizationZIADK015602 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI LEI, ELISSA · 2009 to 2025
$24.7M
Genome-wide mapping of histone modificationsZIAHL005801 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ZHAO, KEJI · 2009 to 2025
$24.0M
Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Investigation of an RNA topoisomerase complex involved in Fragile X syndromeZIAAG000689 · NIA · NATIONAL INSTITUTE ON AGING · PI WANG, WEIDONG · 2011 to 2025
$6.9M
ISOLATION OF PROTEIN COMPLEX INVOLVED IN BLOOM SYNDROMEZ01AG000657 · NIA · NATIONAL INSTITUTE ON AGING · PI WANG, WEIDONG · 2000 to 2008
$636k
Intramural NIH HHS Z01 AG000657
6 · The paper itself

Abstract

Topoisomerases solve topological problems during DNA metabolism, but whether they participate in RNA metabolism remains unclear. Top3β represents a family of topoisomerases carrying activities for both DNA and RNA. Here we show that in Drosophila, Top3β interacts biochemically and genetically with the RNAi-induced silencing complex (RISC) containing AGO2, p68 RNA helicase, and FMRP. Top3β and RISC mutants are similarly defective in heterochromatin formation and transcriptional silencing by position-effect variegation assay. Moreover, both Top3β and AGO2 mutants exhibit reduced levels of heterochromatin protein HP1 in heterochromatin. Furthermore, expression of several genes and transposable elements in heterochromatin is increased in the Top3β mutant. Notably, Top3β mutants defective in either RNA binding or catalytic activity are deficient in promoting HP1 recruitment and silencing of transposable elements. Our data suggest that Top3β may act as an RNA topoisomerase in siRNA-guided heterochromatin formation and transcriptional silencing.

Indexed as

AnimalsArgonaute ProteinsChromosomal Proteins, Non-HistoneDEAD-box RNA HelicasesDNA Topoisomerases, Type IDrosophila melanogasterDrosophila ProteinsFragile X Messenger Ribonucleoprotein 1HeterochromatinProtein BindingRNA-Induced Silencing ComplexRNA InterferenceRNA, Small InterferingAGO2 protein, DrosophilaArgonaute ProteinsChromosomal Proteins, Non-HistoneDEAD-box RNA HelicasesDNA Topoisomerases, Type IDrosophila ProteinsFragile X Messenger Ribonucleoprotein 1Heterochromatinheterochromatin protein 1, DrosophilaRNA-Induced Silencing ComplexRNA, Small Interfering

Identifiers

PMID30470739
PMCPMC6251927
OpenAlexW2900756228

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.