Evidence map›Paper›PMID 26294688›Full record

ArticleGenome research2015

DIS3 shapes the RNA polymerase II transcriptome in humans by degrading a variety of unwanted transcripts.

Teresa Szczepińska, Katarzyna Kalisiak, Rafal Tomecki, Anna Labno, Lukasz S Borowski, Tomasz M Kulinski, Dorota Adamska, Joanna Kosinska, Andrzej Dziembowski

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing 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

55 citing papers in PubMed, 96 citations in OpenAlex.

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  9. Life science alliance · 2024
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  12. SnoRNAs: Exploring Their Implication in Human Diseases.International journal of molecular sciences · 2024
    Review
  13. Haematologica · 2024
    Article
  14. Observational
  15. Article
  16. International journal of molecular sciences · 2023
    Review
  17. 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 2 institutions in 1 country.

Teresa SzczepińskaInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Katarzyna KalisiakInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Rafal TomeckiInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Anna LabnoInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Lukasz S BorowskiInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Tomasz M KulinskiInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Dorota AdamskaInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Joanna KosinskaDepartment of Medical Genetics, Center for Biostructure Research, Medical University of Warsaw, 02-106 Warsaw, Poland.
Andrzej DziembowskiInstitute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland; Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw, 02-106 Warsaw, Poland;
Institute of Biochemistry and Biophysics, Polish Academy of Sciences · PLMedical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human DIS3, the nuclear catalytic subunit of the exosome complex, contains exonucleolytic and endonucleolytic active domains. To identify DIS3 targets genome-wide, we combined comprehensive transcriptomic analyses of engineered HEK293 cells that expressed mutant DIS3, with Photoactivatable Ribonucleoside-Enhanced Cross-Linking and Immunoprecipitation (PAR-CLIP) experiments. In cells expressing DIS3 with both catalytic sites mutated, RNAs originating from unannotated genomic regions increased ∼2.5-fold, covering ∼70% of the genome and allowing for thousands of novel transcripts to be discovered. Previously described pervasive transcription products, such as Promoter Upstream Transcripts (PROMPTs), accumulated robustly upon DIS3 dysfunction, representing a significant fraction of PAR-CLIP reads. We have also detected relatively long putative premature RNA polymerase II termination products of protein-coding genes whose levels in DIS3 mutant cells can exceed the mature mRNAs, indicating that production of such truncated RNA is a common phenomenon. In addition, we found DIS3 to be involved in controlling the formation of paraspeckles, nuclear bodies that are organized around NEAT1 lncRNA, whose short form was overexpressed in cells with mutated DIS3. Moreover, the DIS3 mutations resulted in misregulation of expression of ∼50% of transcribed protein-coding genes, probably as a secondary effect of accumulation of various noncoding RNA species. Finally, cells expressing mutant DIS3 accumulated snoRNA precursors, which correlated with a strong PAR-CLIP signal, indicating that DIS3 is the main snoRNA-processing enzyme. EXOSC10 (RRP6) instead controls the levels of the mature snoRNAs. Overall, we show that DIS3 has a major nucleoplasmic function in shaping the human RNA polymerase II transcriptome.

Indexed as

Transcription, GeneticTranscriptomeExosome Multienzyme Ribonuclease ComplexGene Expression RegulationHEK293 CellsHumansMutant ProteinsRNA, Long NoncodingRNA, MessengerRNA Polymerase IISequence Analysis, RNADIS3 protein, humanExosome Multienzyme Ribonuclease ComplexMutant ProteinsNEAT1 long non-coding RNA, humanRNA, Long NoncodingRNA, MessengerRNA Polymerase II

Identifiers

PMID26294688
PMCPMC4617959
OpenAlexW2216658435

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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.