Evidence map›Paper›PMID 33141022›Full record

ArticleeLife2020

The RIF1-long splice variant promotes G1 phase 53BP1 nuclear bodies to protect against replication stress.

Lotte P Watts, Toyoaki Natsume, Yuichiro Saito, Javier Garzon, Qianqian Dong, Lora Boteva, Nick Gilbert, Masato T Kanemaki, Shin-Ichiro Hiraga, Anne D Donaldson

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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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 3 institutions in 2 countries.

Lotte P WattsInstitute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.ORCID 0000-0002-1364-4345
Toyoaki NatsumeDepartment of Chromosome Science, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.ORCID 0000-0002-3544-4491
Yuichiro SaitoDepartment of Chromosome Science, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.
Javier GarzonInstitute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.
Qianqian DongInstitute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.
Lora BotevaMRC Human Genetics Unit, The University of Edinburgh, Edinburgh, United Kingdom.
Nick GilbertMRC Human Genetics Unit, The University of Edinburgh, Edinburgh, United Kingdom.
Masato T KanemakiDepartment of Chromosome Science, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.ORCID 0000-0002-7657-1649
Shin-Ichiro HiragaInstitute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.ORCID 0000-0002-8722-3869
Anne D DonaldsonInstitute of Medical Sciences, University of Aberdeen, Aberdeen, United Kingdom.ORCID 0000-0001-7842-8136
University of Aberdeen · GBNational Institute of Genetics · JPInstitute of Genetics and Cancer · GB

Funding

Cancer Research UK 19059Cancer Research UK C1445/A19059Cancer Research UK C1445/A20596Medical Research Council MC_UU_00007/13
6 · The paper itself

Abstract

Human cells lacking RIF1 are highly sensitive to replication inhibitors, but the reasons for this sensitivity have been enigmatic. Here, we show that RIF1 must be present both during replication stress and in the ensuing recovery period to promote cell survival. Of two isoforms produced by alternative splicing, we find that RIF1-Long alone can protect cells against replication inhibition, but RIF1-Short is incapable of mediating protection. Consistent with this isoform-specific role, RIF1-Long is required to promote the formation of the 53BP1 nuclear bodies that protect unrepaired damage sites in the G1 phase following replication stress. Overall, our observations show that RIF1 is needed at several cell cycle stages after replication insult, with the RIF1-Long isoform playing a specific role during the ensuing G1 phase in damage site protection.

Indexed as

DNA ReplicationG1 PhaseCell CycleCell LineCell NucleusHumansProtein IsoformsRNA SplicingTelomere-Binding ProteinsTumor Suppressor p53-Binding Protein 1Protein IsoformsRif1 protein, humanTelomere-Binding ProteinsTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1cell biologychromosomesDNA replicationgene expressionhumanreplication stresssplicing

Identifiers

PMID33141022
PMCPMC7671687
OpenAlexW3094871531

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.