Evidence map›Paper›PMID 21497085›Full record

ArticleCurrent biology : CB2011

Oocyte-specific differences in cell-cycle control create an innate susceptibility to meiotic errors.

So Iha Nagaoka, Craig A Hodges, David F Albertini, Patricia Ann Hunt

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
7.5field-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

99 citing papers in PubMed, 172 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Assessment of Chromosome Congression Defects in Mammalian Oocytes.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Can Nicotinamide Adenine Dinucleotide (NADAnimals : an open access journal from MDPI · 2024
    Review
  13. Review
  14. The signal that stimulates mammalian embryo development.Frontiers in cell and developmental biology · 2024
    Review
  15. Early onset of APC/C activity renders SAC inefficient in mouse embryos.Frontiers in cell and developmental biology · 2024
    Article
  16. Article
  17. The large cytoplasmic volume of oocyte.The Journal of reproduction and development · 2023
    Review
  18. Review
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

So Iha NagaokaSchool of Molecular Biosciences and Center for Reproductive Biology, Washington State University, Pullman, WA 99163, USA.
Craig A Hodges
David F Albertini
Patricia Ann Hunt
Washington State University · USCase Western Reserve University · USThe University of Kansas Cancer Center · US

Funding

Translational Research in Cystic FibrosisP30DK027651 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI DRUMM, MITCHELL L · 1986 to 2014
$15.6M
TRAINING IN BIOTECHNOLOGY: EMPHASIS ON PROTEIN CHEMISTRYT32GM008336 · NIGMS · WASHINGTON STATE UNIVERSITY · PI CALL, DOUGLAS R. · 1989 to 2023
$8.9M
GENETIC CONTROL OF MEIOTIC CHROMOSOME SEGREGATIONR01HD037502 · NICHD · WASHINGTON STATE UNIVERSITY · PI HUNT, PATRICIA · 2000 to 2009
$2.8M
CLINICAL PHARMACOLOGY TRAINING GRANTT32GM008386 · NIGMS · GEORGETOWN UNIVERSITY · PI BROWN, MILTON L. · 1990 to 2009
$1.3M
NICHD NIH HHS HD37502NICHD NIH HHS R01 HD037502NIDDK NIH HHS P30 DK027651NIGMS NIH HHS T32 GM008336NIGMS NIH HHS T32 GM008386NIGMS NIH HHS T32GM08386
6 · The paper itself

Abstract

Segregation of homologs at the first meiotic division (MI) is facilitated by crossovers and by a physical constraint imposed on sister kinetochores that facilitates monopolar attachment to the MI spindle. Recombination failure or premature separation of homologs results in univalent chromosomes at MI, and univalents constrained to form monopolar attachments should be inherently unstable and trigger the spindle assembly checkpoint (SAC). Although univalents trigger cell-cycle arrest in the male, this is not the case in mammalian oocytes. Because the spindle assembly portion of the SAC appears to function normally, two hypotheses have been proposed to explain the lack of response to univalents: (1) reduced stringency of the oocyte SAC to aberrant chromosome behavior, and (2) the ability of univalents to satisfy the SAC by forming bipolar attachments. The present study of Mlh1 mutant mice demonstrates that metaphase alignment is not a prerequisite for anaphase onset and provides strong evidence that MI spindle stabilization and anaphase onset require stable bipolar attachment of a critical mass--but not all--of chromosomes. We postulate that subtle differences in SAC-mediated control make the human oocyte inherently error prone and contribute to the age-related increase in aneuploidy.

Indexed as

Chromosome SegregationMeiosisAdaptor Proteins, Signal TransducingAneuploidyAnimalsCell CycleCellular SenescenceChromosomes, MammalianFemaleKinetochoresMiceMice, Inbred C3HMutL Protein Homolog 1Nuclear ProteinsOocytesSex CharacteristicsAdaptor Proteins, Signal TransducingMlh1 protein, mouseMutL Protein Homolog 1Nuclear Proteins

Identifiers

PMID21497085
PMCPMC3225230
OpenAlexW2099544293

What OpenQuestion holds

Textmetadata
LicenceTDM
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.