Evidence map›Paper›PMID 34818558›Full record

ArticleCell reports2021

SUMO orchestrates multiple alternative DNA-protein crosslink repair pathways.

Nataliia Serbyn, Ivona Bagdiul, Audrey Noireterre, Agnès H Michel, Raymond T Suhandynata, Huilin Zhou, Benoît Kornmann, Françoise Stutz

Abstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
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  8. Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. SUMOylation targeting mitophagy in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
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.

Nataliia SerbynDepartment of Cell Biology, University of Geneva, 1211 Geneva 4, Switzerland. Electronic address: nataliia.serbyn@unige.ch.
Ivona BagdiulDepartment of Cell Biology, University of Geneva, 1211 Geneva 4, Switzerland.
Audrey NoireterreDepartment of Cell Biology, University of Geneva, 1211 Geneva 4, Switzerland.
Agnès H MichelInstitute of Biochemistry, ETH Zürich, 8093 Zurich, Switzerland; Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Raymond T SuhandynataDepartment of Cellular and Molecular Medicine, Moores Cancer Center, University of California School of Medicine, San Diego, La Jolla, CA, USA.
Huilin ZhouDepartment of Cellular and Molecular Medicine, Moores Cancer Center, University of California School of Medicine, San Diego, La Jolla, CA, USA.
Benoît KornmannInstitute of Biochemistry, ETH Zürich, 8093 Zurich, Switzerland; Department of Biochemistry, University of Oxford, Oxford OX1 3QU, UK.
Françoise StutzDepartment of Cell Biology, University of Geneva, 1211 Geneva 4, Switzerland. Electronic address: francoise.stutz@unige.ch.

Funding

Contemporary Approaches to Cancer Cell Signaling and CommunicationT32CA009523 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DONOGHUE, DANIEL J, YANG, JING · 1985 to 2025
$12.1M
Suppression of duplication-mediated genome rearrangements by protein sumoylationR01GM116897 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ZHOU, HUILIN · 2015 to 2023
$2.6M
Orbitrap Fusion Mass SpectrometerS10OD023498 · OD · LUDWIG INSTITUTE FOR CANCER RES LTD · PI ZHOU, HUILIN · 2017 to 2017
$600k
NCI NIH HHS T32 CA009523NIGMS NIH HHS R01 GM116897NIH HHS S10 OD023498Wellcome TrustWellcome Trust 214291/Z/18/Z
6 · The paper itself

Abstract

Endogenous metabolites, environmental agents, and therapeutic drugs promote formation of covalent DNA-protein crosslinks (DPCs). Persistent DPCs compromise genome integrity and are eliminated by multiple repair pathways. Aberrant Top1-DNA crosslinks, or Top1ccs, are processed by Tdp1 and Wss1 functioning in parallel pathways in Saccharomyces cerevisiae. It remains obscure how cells choose between diverse mechanisms of DPC repair. Here, we show that several SUMO biogenesis factors (Ulp1, Siz2, Slx5, and Slx8) control repair of Top1cc or an analogous DPC lesion. Genetic analysis reveals that SUMO promotes Top1cc processing in the absence of Tdp1 but has an inhibitory role if cells additionally lack Wss1. In the tdp1Δ wss1Δ mutant, the E3 SUMO ligase Siz2 stimulates sumoylation in the vicinity of the DPC, but not SUMO conjugation to Top1. This Siz2-dependent sumoylation inhibits alternative DPC repair mechanisms, including Ddi1. Our findings suggest that SUMO tunes available repair pathways to facilitate faithful DPC repair.

Indexed as

Cysteine EndopeptidasesDNADNA-Binding ProteinsDNA RepairDNA Topoisomerases, Type IPhosphoric Diester HydrolasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinSumoylationUbiquitin-Protein LigasesCysteine EndopeptidasesDNADNA-Binding ProteinsDNA Topoisomerases, Type IPhosphoric Diester HydrolasesSaccharomyces cerevisiae ProteinsSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinTdp1 protein, S cerevisiaeTOP1 protein, S cerevisiaeUbiquitin-Protein LigasesULP1 protein, S cerevisiaeWSS1 protein, S cerevisiaeDNA-protein crosslinkDPC repairFlp-nickSiz2STUbLSUMOTdp1Top1Top1ccUlp1Wss1

Identifiers

PMID34818558
PMCPMC10042627

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Registered trials

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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.