Evidence map›Paper›PMID 25329383›Full record

ArticlePLoS genetics2014

The chromosomal association of the Smc5/6 complex depends on cohesion and predicts the level of sister chromatid entanglement.

Kristian Jeppsson, Kristian K Carlborg, Ryuichiro Nakato, Davide G Berta, Ingrid Lilienthal, Takaharu Kanno, Arne Lindqvist, Maartje C Brink, Nico P Dantuma, Yuki Katou and 2 more

Abstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed.

  1. Article
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  9. Review
  10. Biology · 2022
    Article
  11. Smc5/6 silences episomal transcription by a three-step function.Nature structural & molecular biology · 2022
    Article
  12. Article
  13. Review
  14. Article
  15. 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

12 authors.

Kristian JeppssonKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Kristian K CarlborgKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Ryuichiro NakatoUniversity of Tokyo, Institute of Molecular and Cellular Biosciences, Laboratory of Genome Structure and Function Center for Epigenetic Disease, Bunkyo-ku, Tokyo, Japan.
Davide G BertaKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Ingrid LilienthalKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Takaharu KannoKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Arne LindqvistKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Maartje C BrinkKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Nico P DantumaKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.
Yuki KatouUniversity of Tokyo, Institute of Molecular and Cellular Biosciences, Laboratory of Genome Structure and Function Center for Epigenetic Disease, Bunkyo-ku, Tokyo, Japan.
Katsuhiko ShirahigeUniversity of Tokyo, Institute of Molecular and Cellular Biosciences, Laboratory of Genome Structure and Function Center for Epigenetic Disease, Bunkyo-ku, Tokyo, Japan.
Camilla SjögrenKarolinska Institutet, Department of Cell and Molecular Biology, Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cohesin complex, which is essential for sister chromatid cohesion and chromosome segregation, also inhibits resolution of sister chromatid intertwinings (SCIs) by the topoisomerase Top2. The cohesin-related Smc5/6 complex (Smc5/6) instead accumulates on chromosomes after Top2 inactivation, known to lead to a buildup of unresolved SCIs. This suggests that cohesin can influence the chromosomal association of Smc5/6 via its role in SCI protection. Using high-resolution ChIP-sequencing, we show that the localization of budding yeast Smc5/6 to duplicated chromosomes indeed depends on sister chromatid cohesion in wild-type and top2-4 cells. Smc5/6 is found to be enriched at cohesin binding sites in the centromere-proximal regions in both cell types, but also along chromosome arms when replication has occurred under Top2-inhibiting conditions. Reactivation of Top2 after replication causes Smc5/6 to dissociate from chromosome arms, supporting the assumption that Smc5/6 associates with a Top2 substrate. It is also demonstrated that the amount of Smc5/6 on chromosomes positively correlates with the level of missegregation in top2-4, and that Smc5/6 promotes segregation of short chromosomes in the mutant. Altogether, this shows that the chromosomal localization of Smc5/6 predicts the presence of the chromatid segregation-inhibiting entities which accumulate in top2-4 mutated cells. These are most likely SCIs, and our results thus indicate that, at least when Top2 is inhibited, Smc5/6 facilitates their resolution.

Indexed as

Binding SitesCell Cycle ProteinsChromatidsChromosomal Proteins, Non-HistoneChromosome SegregationChromosomes, FungalCohesinsDNA BreaksDNA Topoisomerases, Type IIRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseTemperatureCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNA Topoisomerases, Type IISaccharomyces cerevisiae ProteinsSMC5 protein, S cerevisiaeSMC6 protein, S cerevisiae

Identifiers

PMID25329383
PMCPMC4199498

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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.