Evidence map›Paper›PMID 16478984›Full record

ArticleMolecular and cellular biology2006

The Nse5-Nse6 dimer mediates DNA repair roles of the Smc5-Smc6 complex.

Stephanie Pebernard, James Wohlschlegel, W Hayes McDonald, John R Yates, Michael N Boddy

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

93 citing papers in PubMed, 144 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Diploidy confers genomic instability inbioRxiv : the preprint server for biology · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Molecular basis for Nse5-6 mediated regulation of Smc5/6 functions.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. DNA segment capture by Smc5/6 holocomplexes.Nature structural & molecular biology · 2023
    Article
  17. Article
  18. Smc5/6 silences episomal transcription by a three-step function.Nature structural & molecular biology · 2022
    Article
  19. Loss of NSE-4 Perturbs Genome Stability and DNA Repair inInternational journal of molecular sciences · 2022
    Article
  20. Smc5/6 Complex Promotes Rad3Molecular and cellular biology · 2022
    Article

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Stephanie PebernardThe Scripps Research Institute, Rm. MB107, 10550 North Torrey Pines Rd., Molecular Biology, MB-3, La Jolla, CA 92037, USA.
James Wohlschlegel
W Hayes McDonald
John R Yates
Michael N Boddy
Scripps Research Institute · US

Funding

ZDS2P REGULATES SWE1P-DEPENDENT POLARIZED CELL GROWTH IN S CEREVISIAEP41RR011823 · NCRR · UNIVERSITY OF WASHINGTON · PI DAVIS, TRACY · 1996 to 2011
$24.7M
Studies of the Rad60-Smc5-Smc6 DNA Repair ComplexR01GM068608 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI BODDY, MICHAEL N · 2003 to 2020
$6.2M
NCRR NIH HHS P41 RR011823NCRR NIH HHS RR11823NIGMS NIH HHS GM068608NIGMS NIH HHS R01 GM068608
6 · The paper itself

Abstract

Stabilization and processing of stalled replication forks is critical for cell survival and genomic integrity. We characterize a novel DNA repair heterodimer of Nse5 and Nse6, which are nonessential nuclear proteins critical for chromosome segregation in fission yeast. The Nse5/6 dimer facilitates DNA repair as part of the Smc5-Smc6 holocomplex (Smc5/6), the basic architecture of which we define. Nse5-Nse6 [corrected] (Nse5 and Nse6) [corrected] mutants display a high level of spontaneous DNA damage and mitotic catastrophe in the absence of the master checkpoint regulator Rad3 (hATR). Nse5/6 mutants are required for the response to genotoxic agents that block the progression of replication forks, acting in a pathway that allows the tolerance of irreparable UV lesions. Interestingly, the UV sensitivity of Nse5/6 [corrected] is suppressed by concomitant deletion of the homologous recombination repair factor, Rhp51 (Rad51). Further, the viability of Nse5/6 mutants depends on Mus81 and Rqh1, factors that resolve or prevent the formation of Holliday junctions. Consistently, the UV sensitivity of cells lacking Nse5/6 can be partially suppressed by overexpressing the bacterial resolvase RusA. We propose a role for Nse5/6 mutants in suppressing recombination that results in Holliday junction formation or in Holliday junction resolution.

Indexed as

Carrier ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneDimerizationDNA-Binding ProteinsDNA HelicasesDNA RepairDNA ReplicationEndonucleasesEscherichia coli ProteinsGenome, FungalGenomic InstabilityHolliday Junction ResolvasesMultiprotein ComplexesMutationNuclear ProteinsCarrier ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneDNA-Binding ProteinsDNA HelicasesEndonucleasesEscherichia coli ProteinsHolliday Junction ResolvasesMultiprotein ComplexesMUS81 protein, S pombeNse5 protein, S pombeNse6 protein, S pombeNuclear ProteinsRecombinant ProteinsRqh1 protein, S pombeRusA protein, E coliSchizosaccharomyces pombe ProteinsSmc5 protein, S pombesmc6 protein, S pombe

Identifiers

PMID16478984
PMCPMC1430260
OpenAlexW2105092291

What OpenQuestion holds

Textmetadata
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.