Evidence map›Paper›PMID 22513372›Full record

ArticleDevelopment (Cambridge, England)2012

Spindle assembly checkpoint signalling is uncoupled from chromosomal position in mouse oocytes.

Liming Gui, Hayden Homer

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 154 citations in OpenAlex.

  1. Review
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  11. Kinesin motor KIF16A regulates microtubule stability and actin-dependent spindle migration in mouse oocyte meiosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  12. Article
  13. Review
  14. Early onset of APC/C activity renders SAC inefficient in mouse embryos.Frontiers in cell and developmental biology · 2024
    Article
  15. Review
  16. Article
  17. Article
  18. The large cytoplasmic volume of oocyte.The Journal of reproduction and development · 2023
    Review
  19. Article
  20. Insufficient HtrA2 causes meiotic defects in aging germinal vesicle oocytes.Reproductive biology and endocrinology : RB&E · 2022
    Article

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

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.

Liming GuiCell and Developmental Biology, University College London, London WC1E 6BT, UK.
Hayden Homer
University College London · GB

Funding

Wellcome TrustWellcome Trust 082587/Z/07/Z
6 · The paper itself

Abstract

The spindle assembly checkpoint (SAC) averts aneuploidy by coordinating proper bipolar chromosomal attachment with anaphase-promoting complex/cyclosome (APC/C)-mediated securin and cyclin B1 destruction required for anaphase onset. The generation of a Mad2-based signal at kinetochores is central to current models of SAC-based APC/C inhibition. During mitosis, kinetochores of polar-displaced chromosomes, which are at greatest risk of mis-segregating, recruit the highest levels of Mad2, thereby ensuring that SAC activation is proportionate to aneuploidy risk. Paradoxically, although an SAC operates in mammalian oocytes, meiosis I (MI) is notoriously error prone and polar-displaced chromosomes do not prevent anaphase onset. Here we find that Mad2 is not preferentially recruited to the kinetochores of polar chromosomes of wild-type mouse oocytes, in which polar chromosomes are rare, or of oocytes depleted of the kinesin-7 motor CENP-E, in which polar chromosomes are more abundant. Furthermore, in CENP-E-depleted oocytes, although polar chromosomal displacement intensified during MI and the capacity to form stable end-on attachments was severely compromised, all kinetochores nevertheless became devoid of Mad2. Thus, it is possible that the ability of the SAC to robustly discriminate chromosomal position might be compromised by the propensity of oocyte kinetochores to become saturated with unproductive attachments, thereby predisposing to aneuploidy. Our data also reveal novel functions for CENP-E in oocytes: first, CENP-E stabilises BubR1, thereby impacting MI progression; and second, CENP-E mediates bi-orientation by promoting kinetochore reorientation and preventing chromosomal drift towards the poles.

Indexed as

Anaphase-Promoting Complex-CyclosomeAnimalsBlotting, WesternCarrier ProteinsCell Cycle ProteinsChromosomal Proteins, Non-HistoneChromosome SegregationCyclin B1Fluorescent Antibody TechniqueImmunohistochemistryKinetochoresMad2 ProteinsMiceMorpholinosM Phase Cell Cycle CheckpointsOocytesAnaphase-Promoting Complex-CyclosomeBub1b protein, mouseBub1 spindle checkpoint proteinCarrier ProteinsCell Cycle Proteinscentromere protein EChromosomal Proteins, Non-HistoneCyclin B1Mad2l1 protein, mouseMad2 ProteinsMorpholinosProtein Serine-Threonine KinasesSecurinUbiquitin-Protein Ligase Complexes

Identifiers

PMID22513372
PMCPMC3347686
OpenAlexW2039407046

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.