Evidence map›Paper›PMID 29360860›Full record

ArticlePLoS genetics2018

Acute Smc5/6 depletion reveals its primary role in rDNA replication by restraining recombination at fork pausing sites.

Xiao P Peng, Shelly Lim, Shibai Li, Lisette Marjavaara, Andrei Chabes, Xiaolan Zhao

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  7. The Phenotype ofGenes · 2025
    Article
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  12. Review
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  14. Review
  15. Article
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  17. Article
  18. Smc5/6 Complex Promotes Rad3Molecular and cellular biology · 2022
    Article
  19. Article
  20. Article
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

6 authors at 2 institutions in 2 countries.

Xiao P PengMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States of America.ORCID 0000-0002-7738-1150
Shelly LimMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States of America.ORCID 0000-0003-0051-3132
Shibai LiMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States of America.
Lisette MarjavaaraDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.
Andrei ChabesDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.ORCID 0000-0003-1708-8259
Xiaolan ZhaoMolecular Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY, United States of America.
Memorial Sloan Kettering Cancer Center · USUmeå University · SE

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
The Rtt107 interactome structures and functionsR01GM080670 · NIGMS · SLOAN-KETTERING INST CAN RESEARCH · PI ZHAO, XIAOLAN · 2007 to 2021
$4.5M
NCI NIH HHS P30 CA008748NIGMS NIH HHS R01 GM080670
6 · The paper itself

Abstract

Smc5/6, a member of the conserved SMC family of complexes, is essential for growth in most organisms. Its exact functions in a mitotic cell cycle are controversial, as chronic Smc5/6 loss-of-function alleles produce varying phenotypes. To circumvent this issue, we acutely depleted Smc5/6 in budding yeast and determined the first cell cycle consequences of Smc5/6 removal. We found a striking primary defect in replication of the ribosomal DNA (rDNA) array. Each rDNA repeat contains a programmed replication fork barrier (RFB) established by the Fob1 protein. Fob1 removal improves rDNA replication in Smc5/6 depleted cells, implicating Smc5/6 in the management of programmed fork pausing. A similar improvement is achieved by removing the DNA helicase Mph1 whose recombinogenic activity can be inhibited by Smc5/6 under DNA damage conditions. DNA 2D gel analyses further show that Smc5/6 loss increases recombination structures at RFB regions; moreover, mph1∆ and fob1∆ similarly reduce this accumulation. These findings point to an important mitotic role for Smc5/6 in restraining recombination events when protein barriers in rDNA stall replication forks. As rDNA maintenance influences multiple essential cellular processes, Smc5/6 likely links rDNA stability to overall mitotic growth.

Indexed as

DNA ReplicationCell Cycle ProteinsChromosomes, FungalDEAD-box RNA HelicasesDNA-Binding ProteinsDNA DamageDNA, FungalDNA, RibosomalMutationRecombination, GeneticSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCell Cycle ProteinsDEAD-box RNA HelicasesDNA-Binding ProteinsDNA, FungalDNA, RibosomalFOB1 protein, S cerevisiaeMPH1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSMC5 protein, S cerevisiaeSMC6 protein, S cerevisiae

Identifiers

PMID29360860
PMCPMC5779651
OpenAlexW2784488947

What OpenQuestion holds

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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.