Evidence map›Paper›PMID 21976700›Full record

ArticleMolecular biology of the cell2011

Nse1-dependent recruitment of Smc5/6 to lesion-containing loci contributes to the repair defects of mutant complexes.

Claudia Tapia-Alveal, Matthew J O'Connell

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. A SWI/SNF subunit regulates chromosomal dissociation of structural maintenance complex 5 during DNA repair in plant cells.Proceedings of the National Academy of Sciences of the United States of America · 2019
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  14. The CINs of the centromere.Biochemical Society transactions · 2013
    Review
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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

2 authors at 1 institution in 1 country.

Claudia Tapia-AlvealDepartment of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA.
Matthew J O'Connell
Icahn School of Medicine at Mount Sinai · US

Funding

Chk1 signaling in the G2 DNA damage checkpointR01CA100076 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI O'CONNELL, MATTHEW J · 2003 to 2007
$1.7M
Regulation of chromosome segregation by SMC complexes and Top2 in S. pombeR01GM088162 · NIGMS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI O'CONNELL, MATTHEW J · 2011 to 2015
$1.5M
Chk1 signaling in the G2 DNA damage checkpointR56CA100076 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI O'CONNELL, MATTHEW J · 2009 to 2009
$336k
NCI NIH HHS CA100076NCI NIH HHS R01 CA100076NCI NIH HHS R56 CA100076NIGMS NIH HHS GM088162NIGMS NIH HHS R01 GM088162
6 · The paper itself

Abstract

Of the three structural maintenance of chromosomes (SMC) complexes, Smc5/6 remains the most poorly understood. Genetic studies have shown that Smc5/6 mutants are defective in homologous recombination (HR), and consistent with this, Smc5/6 is enriched at lesions. However, Smc5/6 is essential for viability, but HR is not, and the terminal phenotype of null Smc5/6 mutants is mitotic failure. Here we analyze the function of Nse1, which contains a variant RING domain that is characteristic of ubiquitin ligases. Whereas deletion of this domain causes DNA damage sensitivity and mitotic failure, serine mutations in conserved cysteines do not. However, these mutations suppress the DNA damage sensitivity of Smc5/6 hypomorphs but not that of HR mutants and remarkably decrease the recruitment of Smc5/6 to loci containing lesions marked for HR-mediated repair. Analysis of DNA repair pathways in suppressed double mutants suggests that lesions are channeled into recombination-dependent and error-free postreplication repair. Thus the HR defect in Smc5/6 mutants appears to be due to the presence of dysfunctional complexes at lesions rather than to reflect an absolute requirement for Smc5/6 to complete HR.

Indexed as

DNA RepairAmino Acid SubstitutionCell Cycle ProteinsChromosomal Proteins, Non-HistoneCysteineDNA-Binding ProteinsDNA DamageDNA HelicasesHomologous RecombinationMitosisNuclear ProteinsPoint MutationProtein Structure, TertiaryRad52 DNA Repair and Recombination ProteinSchizosaccharomycesSchizosaccharomyces pombe ProteinsBrc1 protein, S pombeCell Cycle ProteinsChromosomal Proteins, Non-HistoneCysteineDNA-Binding ProteinsDNA HelicasesNse1 protein, S pombeNuclear ProteinsRad52 DNA Repair and Recombination ProteinRHP55 protein, S pombeSchizosaccharomyces pombe ProteinsSerineSmc5 protein, S pombesmc6 protein, S pombe

Identifiers

PMID21976700
PMCPMC3226483
OpenAlexW2123458244

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.