Evidence map›Paper›PMID 27085807›Full record

ArticleNucleic acids research2016

Two sets of RNAi components are required for heterochromatin formation in trans triggered by truncated transgenes.

Ulrike Götz, Simone Marker, Miriam Cheaib, Karsten Andresen, Simon Shrestha, Dilip A Durai, Karl J Nordström, Marcel H Schulz, Martin Simon

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

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  6. Feeding exogenous dsRNA interferes with endogenous sRNA accumulation in Paramecium.DNA research : an international journal for rapid publication of reports on genes and genomes · 2020
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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 4 institutions in 1 country.

Ulrike GötzMolecular Cell Dynamics Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany Department of Biology, University of Kaiserslautern, Erwin-Schrödinger Straße, Building Nr. 14, 67663 Kaiserslautern, Germany.
Simone MarkerMolecular Cell Dynamics Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany.
Miriam CheaibMolecular Cell Dynamics Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany Department of Biology, University of Kaiserslautern, Erwin-Schrödinger Straße, Building Nr. 14, 67663 Kaiserslautern, Germany.
Karsten AndresenInstitute of Biotechnology and Drug Research, Erwin-Schrödinger-Str. 56, 67663 Kaiserslautern, Germany.
Simon ShresthaMolecular Cell Dynamics Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany Department of Biology, University of Kaiserslautern, Erwin-Schrödinger Straße, Building Nr. 14, 67663 Kaiserslautern, Germany.
Dilip A DuraiCluster of Excellence, Multimodal Computing and Interaction and Max Planck Institute for Informatics Saarland University, Department for Computational Biology and Applied Algorithmics, Campus E1 4, 66123 Saarbrücken, Germany.
Karl J NordströmDepartment for Genetics, Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany.
Marcel H SchulzCluster of Excellence, Multimodal Computing and Interaction and Max Planck Institute for Informatics Saarland University, Department for Computational Biology and Applied Algorithmics, Campus E1 4, 66123 Saarbrücken, Germany.
Martin SimonMolecular Cell Dynamics Saarland University, Centre for Human and Molecular Biology, Campus A2 4, 66123 Saarbrücken, Germany martin.simon@uni-saarland.de.
Saarland University · DEUniversity of Kaiserslautern · DEInstitut für Biotechnologie und Wirkstoff-Forschung · DEMax Planck Institute for Informatics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Across kingdoms, RNA interference (RNAi) has been shown to control gene expression at the transcriptional- or the post-transcriptional level. Here, we describe a mechanism which involves both aspects: truncated transgenes, which fail to produce intact mRNA, induce siRNA accumulation and silencing of homologous loci in trans in the ciliate Paramecium We show that silencing is achieved by co-transcriptional silencing, associated with repressive histone marks at the endogenous gene. This is accompanied by secondary siRNA accumulation, strictly limited to the open reading frame of the remote locus. Our data shows that in this mechanism, heterochromatic marks depend on a variety of RNAi components. These include RDR3 and PTIWI14 as well as a second set of components, which are also involved in post-transcriptional silencing: RDR2, PTIWI13, DCR1 and CID2. Our data indicates differential processing of nascent un-spliced and long, spliced transcripts thus suggesting a hitherto-unrecognized functional interaction between post-transcriptional and co-transcriptional RNAi. Both sets of RNAi components are required for efficient trans-acting RNAi at the chromatin level and our data indicates similar mechanisms contributing to genome wide regulation of gene expression by epigenetic mechanisms.

Indexed as

RNA InterferenceTransgenesChromatin Assembly and DisassemblyDNA-Binding ProteinsEscherichia coliGene Expression ProfilingGene Expression RegulationGene OntologyHeterochromatinMolecular Sequence AnnotationParameciumPlasmidsPolynucleotide AdenylyltransferaseProtozoan ProteinsRNA, Double-StrandedRNA, MessengerDNA-Binding ProteinsHeterochromatinPolynucleotide AdenylyltransferaseProtozoan ProteinsRNA, Double-StrandedRNA, MessengerRNA, Small InterferingTranscription Factors

Identifiers

PMID27085807
PMCPMC4937312
OpenAlexW2339492155

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.