Evidence map›Paper›PMID 31340047›Full record

ArticleNucleic acids research2019

A low-complexity region in human XRN1 directly recruits deadenylation and decapping factors in 5'-3' messenger RNA decay.

Chung-Te Chang, Sowndarya Muthukumar, Ramona Weber, Yevgen Levdansky, Ying Chen, Dipankar Bhandari, Catia Igreja, Lara Wohlbold, Eugene Valkov, Elisa Izaurralde

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

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  20. Dcp2 C-terminaleLife · 2022
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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

10 authors at 1 institution in 1 country.

Chung-Te ChangDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Sowndarya MuthukumarDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Ramona WeberDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Yevgen LevdanskyDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Ying ChenDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Dipankar BhandariDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Catia IgrejaDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Lara WohlboldDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Eugene ValkovDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Elisa IzaurraldeDepartment of Biochemistry, Max Planck Institute for Developmental Biology, Max-Planck-Ring 5, 72076 Tübingen, Germany.
Max Planck Institute for Developmental Biology · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

XRN1 is the major cytoplasmic exoribonuclease in eukaryotes, which degrades deadenylated and decapped mRNAs in the last step of the 5'-3' mRNA decay pathway. Metazoan XRN1 interacts with decapping factors coupling the final stages of decay. Here, we reveal a direct interaction between XRN1 and the CCR4-NOT deadenylase complex mediated by a low-complexity region in XRN1, which we term the 'C-terminal interacting region' or CIR. The CIR represses reporter mRNA deadenylation in human cells when overexpressed and inhibits CCR4-NOT and isolated CAF1 deadenylase activity in vitro. Through complementation studies in an XRN1-null cell line, we dissect the specific contributions of XRN1 domains and regions toward decay of an mRNA reporter. We observe that XRN1 binding to the decapping activator EDC4 counteracts the dominant negative effect of CIR overexpression on decay. Another decapping activator PatL1 directly interacts with CIR and alleviates the CIR-mediated inhibition of CCR4-NOT activity in vitro. Ribosome profiling revealed that XRN1 loss impacts not only on mRNA levels but also on the translational efficiency of many cellular transcripts likely as a consequence of incomplete decay. Our findings reveal an additional layer of direct interactions in a tightly integrated network of factors mediating deadenylation, decapping and 5'-3' exonucleolytic decay.

Indexed as

DNA-Binding ProteinsEndoribonucleasesExoribonucleasesHumansMicrotubule-Associated ProteinsMultiprotein ComplexesNuclear Receptor Subfamily 4, Group A, Member 2ProteinsReceptors, CCR4Repressor ProteinsRNA CapsRNA, MessengerRNA StabilityTrans-ActivatorsTranscription FactorsCCR4 protein, humanCIR1 protein, humanCNOT8 protein, humanDCP1A protein, humanDNA-Binding ProteinsEDC4 protein, humanEndoribonucleasesExoribonucleasesMicrotubule-Associated ProteinsmRNA decapping enzymesMultiprotein ComplexesNR4A2 protein, humanNuclear Receptor Subfamily 4, Group A, Member 2PATL1 protein, humanProteinsReceptors, CCR4Repressor ProteinsRNA CapsRNA, MessengerTrans-ActivatorsTranscription FactorsXRN1 protein, human

Identifiers

PMID31340047
PMCPMC6753473
OpenAlexW2964189590

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.