Evidence map›Paper›PMID 37463936›Full record

ArticleNature communications2023

Regulation of Rad52-dependent replication fork recovery through serine ADP-ribosylation of PolD3.

Frederick Richards, Marta J Llorca-Cardenosa, Jamie Langton, Sara C Buch-Larsen, Noor F Shamkhi, Abhishek Bharadwaj Sharma, Michael L Nielsen, Nicholas D Lakin

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-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

9 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
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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

8 authors at 2 institutions in 2 countries.

Frederick RichardsDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK.
Marta J Llorca-CardenosaDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK.
Jamie LangtonDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK.
Sara C Buch-LarsenNovo Nordisk Foundation Centre for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200, Copenhagen, Denmark.ORCID 0000-0001-6250-5467
Noor F ShamkhiDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK.
Abhishek Bharadwaj SharmaDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK.ORCID 0000-0003-2554-1025
Michael L NielsenNovo Nordisk Foundation Centre for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Blegdamsvej 3B, 2200, Copenhagen, Denmark.ORCID 0000-0002-0067-9039
Nicholas D LakinDepartment of Biochemistry, University of Oxford, South Parks Road, Oxford, UK. nicholas.lakin@bioch.ox.ac.uk.ORCID 0000-0003-4999-5814
University of Oxford · GBUniversity of Copenhagen · DK

Funding

Medical Research Council MR/P018963/1Medical Research Council MR/P028284/1Medical Research Council MR/V00896X/1Medical Research Council MR/W017350/1Wellcome TrustWellcome Trust 102348/Z/13/Z
6 · The paper itself

Abstract

Although Poly(ADP-ribose)-polymerases (PARPs) are key regulators of genome stability, how site-specific ADP-ribosylation regulates DNA repair is unclear. Here, we describe a novel role for PARP1 and PARP2 in regulating Rad52-dependent replication fork repair to maintain cell viability when homologous recombination is dysfunctional, suppress replication-associated DNA damage, and maintain genome stability. Mechanistically, Mre11 and ATM are required for induction of PARP activity in response to replication stress that in turn promotes break-induced replication (BIR) through assembly of Rad52 at stalled/damaged replication forks. Further, by mapping ADP-ribosylation sites induced upon replication stress, we identify that PolD3 is a target for PARP1/PARP2 and that its site-specific ADP-ribosylation is required for BIR activity, replication fork recovery and genome stability. Overall, these data identify a critical role for Mre11-dependent PARP activation and site-specific ADP-ribosylation in regulating BIR to maintain genome integrity during DNA synthesis.

Indexed as

Poly(ADP-ribose) Polymerase InhibitorsSerineADP-RibosylationDNA DamageDNA RepairDNA ReplicationGenomic InstabilityHumansPoly (ADP-Ribose) Polymerase-1Poly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsSerine

Identifiers

PMID37463936
PMCPMC10354178
OpenAlexW4384662447

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.