Evidence map›Paper›PMID 25995189›Full record

ArticleGenes & development2015

Position-specific binding of FUS to nascent RNA regulates mRNA length.

Akio Masuda, Jun-ichi Takeda, Tatsuya Okuno, Takaaki Okamoto, Bisei Ohkawara, Mikako Ito, Shinsuke Ishigaki, Gen Sobue, Kinji Ohno

Abstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing 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

80 citing papers in PubMed.

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20 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

9 authors.

Akio MasudaDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Jun-ichi TakedaDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Tatsuya OkunoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Takaaki OkamotoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Bisei OhkawaraDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Mikako ItoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan;
Shinsuke IshigakiDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Gen SobueDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Kinji OhnoDivision of Neurogenetics, Center for Neurological Diseases and Cancer, Showa-ku, Nagoya 466-8550, Japan; ohnok@med.nagoya-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More than half of all human genes produce prematurely terminated polyadenylated short mRNAs. However, the underlying mechanisms remain largely elusive. CLIP-seq (cross-linking immunoprecipitation [CLIP] combined with deep sequencing) of FUS (fused in sarcoma) in neuronal cells showed that FUS is frequently clustered around an alternative polyadenylation (APA) site of nascent RNA. ChIP-seq (chromatin immunoprecipitation [ChIP] combined with deep sequencing) of RNA polymerase II (RNAP II) demonstrated that FUS stalls RNAP II and prematurely terminates transcription. When an APA site is located upstream of an FUS cluster, FUS enhances polyadenylation by recruiting CPSF160 and up-regulates the alternative short transcript. In contrast, when an APA site is located downstream from an FUS cluster, polyadenylation is not activated, and the RNAP II-suppressing effect of FUS leads to down-regulation of the alternative short transcript. CAGE-seq (cap analysis of gene expression [CAGE] combined with deep sequencing) and PolyA-seq (a strand-specific and quantitative method for high-throughput sequencing of 3' ends of polyadenylated transcripts) revealed that position-specific regulation of mRNA lengths by FUS is operational in two-thirds of transcripts in neuronal cells, with enrichment in genes involved in synaptic activities.

Indexed as

Gene Expression RegulationAnimalsCell Line, TumorCleavage And Polyadenylation Specificity FactorGene Knockdown TechniquesHEK293 CellsHumansMicePolyadenylationProtein BindingRNARNA-Binding Protein FUSRNA, MessengerRNA Polymerase IITranscriptomeCleavage And Polyadenylation Specificity FactorRNARNA-Binding Protein FUSRNA, MessengerRNA Polymerase IIalternative polyadenylationCLIPFUSmRNA lengthRNA polymerase II

Identifiers

PMID25995189
PMCPMC4441052

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Registered trials

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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.