Evidence map›Paper›PMID 36057640›Full record

ArticleNature communications2022

The nucleolus is the site for inflammatory RNA decay during infection.

Taeyun A Lee, Heonjong Han, Ahsan Polash, Seok Keun Cho, Ji Won Lee, Eun A Ra, Eunhye Lee, Areum Park, Sujin Kang, Junhee L Choi and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Targeting the Hippo pathway in Schwann cells ameliorates peripheral nerve degeneration via a polypharmacological mechanism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
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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

19 authors at 6 institutions in 2 countries.

Taeyun A LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Heonjong HanDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Ahsan PolashLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-6591-3164
Seok Keun ChoDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Ji Won LeeDepartment of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangneung, South Korea.
Eun A RaDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Eunhye LeeDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Areum ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Sujin KangDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Junhee L ChoiDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Ji Hyun KimDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, South Korea.
Ji Eun LeeDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, South Korea.
Kyung-Won MinDepartment of Biology, College of Natural Sciences, Gangneung-Wonju National University, Gangneung, South Korea.
Seong Wook YangDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Markus HafnerLaboratory of Muscle Stem Cells and Gene Regulation, National Institute for Arthritis and Musculoskeletal and Skin Disease, National Institutes of Health, Bethesda, MD, USA.ORCID 0000-0002-4336-6518
Insuk LeeDepartment of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea.
Je-Hyun YoonDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, Charleston, SC, USA. yoonje@musc.edu.ORCID 0000-0001-7615-8654
Sungwook LeeDivision of Tumor Immunology, Research Institute, National Cancer Center, Goyang, South Korea. swlee1905@ncc.re.kr.ORCID 0000-0001-8343-8160
Boyoun ParkDepartment of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea. bypark@yonsei.ac.kr.ORCID 0000-0003-4119-3649
Yonsei University · KRGangneung–Wonju National University · KRNational Institutes of Health · USMedical University of South Carolina · USNational Cancer Center · USSamsung (South Korea) · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory cytokines are key signaling molecules that can promote an immune response, thus their RNA turnover must be tightly controlled during infection. Most studies investigate the RNA decay pathways in the cytosol or nucleoplasm but never focused on the nucleolus. Although this organelle has well-studied roles in ribosome biogenesis and cellular stress sensing, the mechanism of RNA decay within the nucleolus is not completely understood. Here, we report that the nucleolus is an essential site of inflammatory pre-mRNA instability during infection. RNA-sequencing analysis reveals that not only do inflammatory genes have higher intronic read densities compared with non-inflammatory genes, but their pre-mRNAs are highly enriched in nucleoli during infection. Notably, nucleolin (NCL) acts as a guide factor for recruiting cytosine or uracil (C/U)-rich sequence-containing inflammatory pre-mRNAs and the Rrp6-exosome complex to the nucleolus through a physical interaction, thereby enabling targeted RNA delivery to Rrp6-exosomes and subsequent degradation. Consequently, Ncl depletion causes aberrant hyperinflammation, resulting in a severe lethality in response to LPS. Importantly, the dynamics of NCL post-translational modifications determine its functional activity in phases of LPS. This process represents a nucleolus-dependent pathway for maintaining inflammatory gene expression integrity and immunological homeostasis during infection.

Indexed as

Cell NucleolusLipopolysaccharidesCell NucleusRNARNA StabilityLipopolysaccharidesRNA

Identifiers

PMID36057640
PMCPMC9440930
OpenAlexW4294433638

What OpenQuestion holds

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LicenceCC BY
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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.