Evidence map›Paper›PMID 30061412›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Warsaw breakage syndrome DDX11 helicase acts jointly with RAD17 in the repair of bulky lesions and replication through abasic sites.

Takuya Abe, Masato Ooka, Ryotaro Kawasumi, Keiji Miyata, Minoru Takata, Kouji Hirota, Dana Branzei

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 8% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  12. DDX11 loss causes replication stress and pharmacologically exploitable DNA repair defects.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  13. Article
  14. Review
  15. Article
  16. Role of the DDX11 DNA Helicase in Warsaw Breakage Syndrome Etiology.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Structure of the human clamp loader reveals an autoinhibited conformation of a substrate-bound AAA+ switch.Proceedings of the National Academy of Sciences of the United States of America · 2020
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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

7 authors at 3 institutions in 2 countries.

Takuya AbeDNA Repair lab, IFOM, Fondazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, 20139 Milan, Italy.
Masato OokaDNA Repair lab, IFOM, Fondazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, 20139 Milan, Italy.
Ryotaro KawasumiDNA Repair lab, IFOM, Fondazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, 20139 Milan, Italy.
Keiji MiyataDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, 192-0397 Tokyo, Japan.
Minoru TakataLaboratory of DNA Damage Signaling, Radiation Biology Center, Kyoto University, 606-8501 Kyoto, Japan.
Kouji HirotaDepartment of Chemistry, Graduate School of Science, Tokyo Metropolitan University, Hachioji-shi, 192-0397 Tokyo, Japan.
Dana BranzeiDNA Repair lab, IFOM, Fondazione Italiana per la Ricerca sul Cancro Institute of Molecular Oncology, 20139 Milan, Italy; dana.branzei@ifom.eu.ORCID 0000-0002-0544-4888
IFOM · ITTokyo Metropolitan University · JPKyoto University · JP

Funding

European Research Council 242928
6 · The paper itself

Abstract

Warsaw breakage syndrome, a developmental disorder caused by mutations in the DDX11/ChlR1 helicase, shows cellular features of genome instability similar to Fanconi anemia (FA). Here we report that DDX11-deficient avian DT40 cells exhibit interstrand crosslink (ICL)-induced chromatid breakage, with DDX11 functioning as backup for the FA pathway in regard to ICL repair. Importantly, we establish that DDX11 acts jointly with the 9-1-1 checkpoint clamp and its loader, RAD17, primarily in a postreplicative fashion, to promote homologous recombination repair of bulky lesions, but is not required for intra-S checkpoint activation or efficient fork progression. Notably, we find that DDX11 also promotes diversification of the chicken Ig-variable gene, a process triggered by programmed abasic sites, by facilitating both hypermutation and homeologous recombination-mediated gene conversion. Altogether, our results uncover that DDX11 orchestrates jointly with 9-1-1 and its loader, RAD17, DNA damage tolerance at sites of bulky lesions, and endogenous abasic sites. These functions may explain the essential roles of DDX11 and its similarity with 9-1-1 during development.

Indexed as

DNA RepairDNA ReplicationAnimalsCell Cycle ProteinsChickensDEAD-box RNA HelicasesDNA HelicasesFanconi AnemiaGenomic InstabilityHomologous RecombinationHumansSomatic Hypermutation, ImmunoglobulinCell Cycle ProteinsDDX11 protein, humanDEAD-box RNA HelicasesDNA HelicasesRad17 protein, humanabasic sitesbulky lesionshomologous recombinationmutagenesisreplication stress

Identifiers

PMID30061412
PMCPMC6099846
OpenAlexW2884273780

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.