Evidence map›Paper›PMID 27056668›Full record

ArticleGenes & development2016

PolySUMOylation by Siz2 and Mms21 triggers relocation of DNA breaks to nuclear pores through the Slx5/Slx8 STUbL.

Chihiro Horigome, Denise E Bustard, Isabella Marcomini, Neda Delgoshaie, Monika Tsai-Pflugfelder, Jennifer A Cobb, Susan M Gasser

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing 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

79 citing papers in PubMed, 127 citations in OpenAlex.

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  14. Multifaceted roles of SUMO in DNA metabolism.Nucleus (Austin, Tex.) · 2024
    Review
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  16. Article
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19 more citing papers are in PubMed but not listed here.

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.

Chihiro HorigomeFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
Denise E BustardDepartment of Biochemistry and Molecular Biology, Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada; Department of Oncology, Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada;
Isabella MarcominiFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland; Faculty of Natural Sciences, University of Basel, CH-4056 Basel, Switzerland.
Neda DelgoshaieFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
Monika Tsai-PflugfelderFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland;
Jennifer A CobbDepartment of Biochemistry and Molecular Biology, Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada; Department of Oncology, Robson DNA Science Centre, Arnie Charbonneau Cancer Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada;
Susan M GasserFriedrich Miescher Institute for Biomedical Research, CH-4058 Basel, Switzerland; Faculty of Natural Sciences, University of Basel, CH-4056 Basel, Switzerland.
Friedrich Miescher Institute · CHUniversity of Calgary · CAUniversity of Basel · CH

Funding

Canadian Institutes of Health Research MOP-82736
6 · The paper itself

Abstract

High-resolution imaging shows that persistent DNA damage in budding yeast localizes in distinct perinuclear foci for repair. The signals that trigger DNA double-strand break (DSB) relocation or determine their destination are unknown. We show here that DSB relocation to the nuclear envelope depends on SUMOylation mediated by the E3 ligases Siz2 and Mms21. In G1, a polySUMOylation signal deposited coordinately by Mms21 and Siz2 recruits the SUMO targeted ubiquitin ligase Slx5/Slx8 to persistent breaks. Both Slx5 and Slx8 are necessary for damage relocation to nuclear pores. When targeted to an undamaged locus, however, Slx5 alone can mediate relocation in G1-phase cells, bypassing the requirement for polySUMOylation. In contrast, in S-phase cells, monoSUMOylation mediated by the Rtt107-stabilized SMC5/6-Mms21 E3 complex drives DSBs to the SUN domain protein Mps3 in a manner independent of Slx5. Slx5/Slx8 and binding to pores favor repair by ectopic break-induced replication and imprecise end-joining.

Indexed as

DNA Breaks, Double-StrandedSumoylationMutationNuclear EnvelopeNuclear PoreProtein BindingSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseSUMO-1 ProteinUbiquitin-Protein LigasesMms21 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSiz2 protein, S cerevisiaeSlx5 protein, S cerevisiaeSlx8 protein, S cerevisiaeSUMO-1 ProteinUbiquitin-Protein LigasesDNA damageMms21nuclear organizationnuclear poresSiz2Slx5SUMO

Identifiers

PMID27056668
PMCPMC4840299
OpenAlexW2323304212

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.