Evidence map›Paper›PMID 24115770›Full record

ArticleGenes & development2013

Dual mechanisms prevent premature chromosome segregation during meiosis.

Seoyoung Kim, Régis Meyer, Hoa Chuong, Dean S Dawson

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed, 41 citations in OpenAlex.

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  20. Multiple Duties for Spindle Assembly Checkpoint Kinases in Meiosis.Frontiers in cell and developmental biology · 2017
    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

4 authors at 2 institutions in 1 country.

Seoyoung KimCell Cycle and Cancer Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA;
Régis Meyer
Hoa Chuong
Dean S Dawson
Oklahoma Medical Research Foundation · USUniversity of Oklahoma Health Sciences Center · US

Funding

Meiotic Centromere Behavior in YeastR01GM087377 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI DAWSON, DEAN S · 2010 to 2017
$2.5M
NIGMS NIH HHS R01 GM087377NIGMS NIH HHS R01GM087377
6 · The paper itself

Abstract

In meiosis I, homologous chromosomes pair and then attach to the spindle so that the homologs can be pulled apart at anaphase I. The segregation of homologs before pairing would be catastrophic. We describe two mechanisms that prevent this. First, in early meiosis, Ipl1, the budding yeast homolog of the mammalian Aurora B kinase, triggers shedding of a kinetochore protein, preventing microtubule attachment. Second, Ipl1 localizes to the spindle pole bodies (SPBs), where it blocks spindle assembly. These processes are reversed upon expression of Ndt80. Previous studies have shown that Ndt80 is expressed when homologs have successfully partnered, and this triggers a rise in the levels of cyclin-dependent kinase (CDK). We found that CDK phosphorylates Ipl1, delocalizing it from SPBs, triggering spindle assembly. At the same time, kinetochores reassemble. Thus, dual mechanisms controlled by Ipl1 and Ntd80 coordinate chromosome and spindle behaviors to prevent the attachment of unpartnered chromosomes to the meiotic spindle.

Indexed as

Aurora KinasesChromosome SegregationCyclin-Dependent KinasesDNA-Binding ProteinsGene Expression Regulation, FungalKinetochoresMeiosisMicrotubulesPhosphorylationProtein TransportSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpindle ApparatusTranscription FactorsAurora KinasesCyclin-Dependent KinasesDNA-Binding ProteinsIPL1 protein, S cerevisiaeNDT80 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsCdc28Clb4Ipl1kinetochoresmeiosisspindle pole body

Identifiers

PMID24115770
PMCPMC3850097
OpenAlexW2158940186

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.