Evidence map›Paper›PMID 27374334›Full record

ArticleCell2016

An Abundant Class of Non-coding DNA Can Prevent Stochastic Gene Silencing in the C. elegans Germline.

Christian Frøkjær-Jensen, Nimit Jain, Loren Hansen, M Wayne Davis, Yongbin Li, Di Zhao, Karine Rebora, Jonathan R M Millet, Xiao Liu, Stuart K Kim and 3 more

Abstract read
In one paragraph

Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
–field-weighted citation impact
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

66 citing papers in PubMed.

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  18. Insights in piRNA targeting rules.Wiley interdisciplinary reviews. RNA · 2023
    Article
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  20. Article

6 more citing papers are in PubMed but not listed here.

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

13 authors.

Christian Frøkjær-JensenDepartment of Biology, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112, USA; Department of Pathology, Stanford University, Stanford, CA 94305, USA; Department of Biomedical Sciences and Danish National Research Foundation Centre for Cardiac Arrhythmia, University of Copenhagen, 2200 Copenhagen N, Denmark.
Nimit JainDepartment of Bioengineering, Stanford University School of Medicine, Stanford, CA 94305, USA.
Loren HansenDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
M Wayne DavisDepartment of Biology, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112, USA.
Yongbin LiSchool of Life Sciences, Tsinghua University, Beijing 100084, China.
Di ZhaoSchool of Life Sciences, Tsinghua University, Beijing 100084, China.
Karine ReboraIECB, University of Bordeaux, Laboratoire ARNA-INSERM, U869, 33600 Pessac, France.
Jonathan R M MilletIECB, University of Bordeaux, Laboratoire ARNA-INSERM, U869, 33600 Pessac, France.
Xiao LiuDepartment of Developmental Biology, Stanford University Medical Center, Stanford, CA 94305, USA; School of Life Sciences, Tsinghua University, Beijing 100084, China.
Stuart K KimDepartment of Developmental Biology, Stanford University Medical Center, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA.
Denis DupuyIECB, University of Bordeaux, Laboratoire ARNA-INSERM, U869, 33600 Pessac, France.
Erik M JorgensenDepartment of Biology, Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112, USA. Electronic address: jorgensen@biology.utah.edu.
Andrew Z FireDepartment of Pathology, Stanford University, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA. Electronic address: afire@stanford.edu.

Funding

GENE REGULATION DURING EARLY DEVELOPMENT OF C. ELEGANSR01GM037706 · NIGMS · STANFORD UNIVERSITY · PI FIRE, ANDREW Z. · 1987 to 2018
$11.0M
Mechanisms of Aging in C. elegansR01AG025941 · NIA · STANFORD UNIVERSITY · PI DAVIS, RONALD WAYNE · 2007 to 2017
$3.1M
Engineering the C. Elegans GenomeR01GM095817 · NIGMS · UNIVERSITY OF UTAH · PI JORGENSEN, ERIK M · 2011 to 2021
$2.8M
Howard Hughes Medical InstituteNIA NIH HHS R01 AG025941NIGMS NIH HHS R01 GM037706NIGMS NIH HHS R01 GM095817
6 · The paper itself

Abstract

Cells benefit from silencing foreign genetic elements but must simultaneously avoid inactivating endogenous genes. Although chromatin modifications and RNAs contribute to maintenance of silenced states, the establishment of silenced regions will inevitably reflect underlying DNA sequence and/or structure. Here, we demonstrate that a pervasive non-coding DNA feature in Caenorhabditis elegans, characterized by 10-base pair periodic An/Tn-clusters (PATCs), can license transgenes for germline expression within repressive chromatin domains. Transgenes containing natural or synthetic PATCs are resistant to position effect variegation and stochastic silencing in the germline. Among endogenous genes, intron length and PATC-character undergo dramatic changes as orthologs move from active to repressive chromatin over evolutionary time, indicating a dynamic character to the An/Tn periodicity. We propose that PATCs form the basis of a cellular immune system, identifying certain endogenous genes in heterochromatic contexts as privileged while foreign DNA can be suppressed with no requirement for a cellular memory of prior exposure.

Indexed as

Gene SilencingAnimalsBase CompositionCaenorhabditis elegansChromatinDNA, IntergenicDNA Transposable ElementsDNA, ViralGerm CellsIntronsPromoter Regions, GeneticRNA, AntisenseRNA, MessengerTransgenesChromatinDNA, IntergenicDNA Transposable ElementsDNA, ViralRNA, AntisenseRNA, Messenger

Identifiers

PMID27374334
PMCPMC4947018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.