Evidence map›Paper›PMID 27128635›Full record

ArticlePLoS genetics2016

A Cohesin-Based Partitioning Mechanism Revealed upon Transcriptional Inactivation of Centromere.

Michael Tsabar, Julian Haase, Benjamin Harrison, Chloe E Snider, Brittany Eldridge, Lila Kaminsky, Rebecca M Hine, James E Haber, Kerry Bloom

Abstract read
In one paragraph

Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Centromere Structure and Function.Progress in molecular and subcellular biology
    Review
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

9 authors.

Michael TsabarDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, United States of America.
Julian HaaseDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Benjamin HarrisonDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Chloe E SniderDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
Brittany EldridgeDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.ORCID http://orcid.org/0000-0003-2000-8301
Lila KaminskyDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, United States of America.
Rebecca M HineDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, United States of America.
James E HaberDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts, United States of America.
Kerry BloomDepartment of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.

Funding

Structure and Function of a Eukaryotic CentromereR01GM032238 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOOM, KERRY S · 1985 to 2025
$6.2M
Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
Structure and Function of a Eukaryotic CentromereR37GM032238 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BLOOM, KERRY S, YEH, ELAINE YING · 2011 to 2020
$5.2M
Arrest, Recovery, and Adaptation from DNA DamageR01GM061766 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2001 to 2016
$4.6M
RECOMBINATION MECHANISMS IN YEAST CELL DIFFERENTIATIONR01GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 1985 to 2006
$3.4M
NIGMS NIH HHS GM20056NIGMS NIH HHS GM32238NIGMS NIH HHS GM61766NIGMS NIH HHS R01 GM020056NIGMS NIH HHS R01 GM032238NIGMS NIH HHS R01 GM061766NIGMS NIH HHS R37 GM020056NIGMS NIH HHS R37 GM032238
6 · The paper itself

Abstract

Transcriptional inactivation of the budding yeast centromere has been a widely used tool in studies of chromosome segregation and aneuploidy. In haploid cells when an essential chromosome contains a single conditionally inactivated centromere (GAL-CEN), cell growth rate is slowed and segregation fidelity is reduced; but colony formation is nearly 100%. Pedigree analysis revealed that only 30% of the time both mother and daughter cell inherit the GAL-CEN chromosome. The reduced segregation capacity of the GAL-CEN chromosome is further compromised upon reduction of pericentric cohesin (mcm21∆), as reflected in a further diminishment of the Mif2 kinetochore protein at GAL-CEN. By redistributing cohesin from the nucleolus to the pericentromere (by deleting SIR2), there is increased presence of the kinetochore protein Mif2 at GAL-CEN and restoration of cell viability. These studies identify the ability of cohesin to promote chromosome segregation via kinetochore assembly, in a situation where the centromere has been severely compromised.

Indexed as

AnaphaseCell Cycle ProteinsCell SurvivalCentromereChromosomal Proteins, Non-HistoneChromosome SegregationCohesinsDNA-Binding ProteinsHaploidyKinetochoresSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpindle ApparatusTranscriptional ActivationCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsMCM21 protein, S cerevisiaeMIF2 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID27128635
PMCPMC4851351

What OpenQuestion holds

Textmetadata
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.