Evidence map›Paper›PMID 26902262›Full record

ArticleEMBO reports2016

Regulating retrotransposon activity through the use of alternative transcription start sites.

Jenna Persson, Babett Steglich, Agata Smialowska, Mette Boyd, Jette Bornholdt, Robin Andersson, Catherine Schurra, Benoit Arcangioli, Albin Sandelin, Olaf Nielsen and 1 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
10.3field-weighted citation impact, top 3% 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

14 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Chromatin remodeller Fun30Nature communications · 2017
    Article
  13. Article
  14. Article
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

11 authors at 3 institutions in 3 countries.

Jenna PerssonDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Babett SteglichDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Agata SmialowskaDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden.
Mette BoydDepartment of Biology, The Bioinformatics Centre, University of Copenhagen, Copenhagen, Denmark Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark.
Jette BornholdtDepartment of Biology, The Bioinformatics Centre, University of Copenhagen, Copenhagen, Denmark Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark.
Robin AnderssonDepartment of Biology, The Bioinformatics Centre, University of Copenhagen, Copenhagen, Denmark.
Catherine SchurraUnite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.
Benoit ArcangioliUnite Dynamique du Génome, Département Génomes et Génétique, Pasteur Institute, Paris, France.
Albin SandelinDepartment of Biology, The Bioinformatics Centre, University of Copenhagen, Copenhagen, Denmark Biotech Research and Innovation Centre, University of Copenhagen, Copenhagen, Denmark.
Olaf NielsenDepartment of Biology, Cell Cycle and Genome Stability Group, University of Copenhagen, Copenhagen, Denmark.
Karl EkwallDepartment of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden karl.ekwall@ki.se.
University of Copenhagen · DKKarolinska Institutet · SEInstitut Pasteur · FR

Funding

European Research Council 638273
6 · The paper itself

Abstract

Retrotransposons, the ancestors of retroviruses, have the potential for gene disruption and genomic takeover if not kept in check. Paradoxically, although host cells repress these elements by multiple mechanisms, they are transcribed and are even activated under stress conditions. Here, we describe a new mechanism of retrotransposon regulation through transcription start site (TSS) selection by altered nucleosome occupancy. We show that Fun30 chromatin remodelers cooperate to maintain a high level of nucleosome occupancy at retrotransposon-flanking long terminal repeat (LTR) elements. This enforces the use of a downstream TSS and the production of a truncated RNA incapable of reverse transcription and retrotransposition. However, in stressed cells, nucleosome occupancy at LTR elements is reduced, and the TSS shifts to allow for productive transcription. We propose that controlled retrotransposon transcription from a nonproductive TSS allows for rapid stress-induced activation, while preventing uncontrolled transposon activity in the genome.

Indexed as

Gene Expression RegulationRetroelementsTranscription Initiation SiteBase SequenceCatalysisChromatinChromatin Assembly and DisassemblyModels, BiologicalMutationNucleosomesPhenotypeStress, PhysiologicalTerminal Repeat SequencesTranscriptional ActivationChromatinNucleosomesRetroelementschromatin remodelingretrotransposable elementstranscriptional regulation

Identifiers

PMID26902262
PMCPMC5341516
OpenAlexW2284683336

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.