Evidence map›Paper›PMID 31782550›Full record

ArticleThe EMBO journal2020

LncRNA-dependent nuclear stress bodies promote intron retention through SR protein phosphorylation.

Kensuke Ninomiya, Shungo Adachi, Tohru Natsume, Junichi Iwakiri, Goro Terai, Kiyoshi Asai, Tetsuro Hirose

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 164 citations in OpenAlex.

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  15. Downregulation of Gene Expression by Alpha Satellite Transcripts.International journal of molecular sciences · 2025
    Article
  16. Review
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  19. Article
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Kensuke NinomiyaInstitute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Shungo AdachiMolecular Profiling Research Center, National Institute for Advanced Industrial Science and Technology (AIST), Tokyo, Japan.ORCID 0000-0001-5232-411X
Tohru NatsumeMolecular Profiling Research Center, National Institute for Advanced Industrial Science and Technology (AIST), Tokyo, Japan.
Junichi IwakiriGraduate School of Frontier Sciences, University of Tokyo, Kashiwa, Japan.
Goro TeraiGraduate School of Frontier Sciences, University of Tokyo, Kashiwa, Japan.
Kiyoshi AsaiGraduate School of Frontier Sciences, University of Tokyo, Kashiwa, Japan.
Tetsuro HiroseInstitute for Genetic Medicine, Hokkaido University, Sapporo, Japan.ORCID 0000-0003-1068-5464
The University of Tokyo · JPHokkaido University · JPNational Institute of Advanced Industrial Science and Technology · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology (MEXT) JP16H06279Ministry of Education, Culture, Sports, Science and Technology (MEXT) JP17H03630Ministry of Education, Culture, Sports, Science and Technology (MEXT) JP17K19335Ministry of Education, Culture, Sports, Science and Technology (MEXT) JP19K06478Ministry of Education, Culture, Sports, Science and Technology (MEXT) JP26113002Tokyo Biochemical Research Foundation (TBRF)
6 · The paper itself

Abstract

A number of long noncoding RNAs (lncRNAs) are induced in response to specific stresses to construct membrane-less nuclear bodies; however, their function remains poorly understood. Here, we report the role of nuclear stress bodies (nSBs) formed on highly repetitive satellite III (HSATIII) lncRNAs derived from primate-specific satellite III repeats upon thermal stress exposure. A transcriptomic analysis revealed that depletion of HSATIII lncRNAs, resulting in elimination of nSBs, promoted splicing of 533 retained introns during thermal stress recovery. A HSATIII-Comprehensive identification of RNA-binding proteins by mass spectrometry (ChIRP-MS) analysis identified multiple splicing factors in nSBs, including serine and arginine-rich pre-mRNA splicing factors (SRSFs), the phosphorylation states of which affect splicing patterns. SRSFs are rapidly de-phosphorylated upon thermal stress exposure. During stress recovery, CDC like kinase 1 (CLK1) was recruited to nSBs and accelerated the re-phosphorylation of SRSF9, thereby promoting target intron retention. Our findings suggest that HSATIII-dependent nSBs serve as a conditional platform for phosphorylation of SRSFs by CLK1 to promote the rapid adaptation of gene expression through intron retention following thermal stress exposure.

Indexed as

Heat-Shock ResponseMicrosatellite RepeatsAnimalsCell NucleusCHO CellsCricetulusExome SequencingGene Expression ProfilingGene Expression RegulationHeLa CellsHumansIntronsPhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, Long NoncodingClk dual-specificity kinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, Long NoncodingRNA Splicing FactorsSerine-Arginine Splicing FactorsSRSF9 protein, humanintron retentionnoncoding RNAnuclear stress bodiesphosphorylationsplicing factors

Identifiers

PMID31782550
PMCPMC6996502
OpenAlexW2989572075

What OpenQuestion holds

Textmetadata
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.