Evidence map›Paper›PMID 20941357›Full record

ArticlePLoS genetics2010

Cdc20 is critical for meiosis I and fertility of female mice.

Fang Jin, Masakazu Hamada, Liviu Malureanu, Karthik B Jeganathan, Wei Zhou, Dean E Morbeck, Jan M van Deursen

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Advances in the genetic etiology of female infertility.Journal of assisted reproduction and genetics · 2024
    Review
  7. The signal that stimulates mammalian embryo development.Frontiers in cell and developmental biology · 2024
    Review
  8. Review
  9. Meiotic Cell Cycle Progression in Mouse Oocytes: Role of Cyclins.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Regulation of oocyte maturation: Role of conserved ERK signaling.Molecular reproduction and development · 2022
    Review
  15. Article
  16. Article
  17. Article
  18. Identification of Novel Mutations inFrontiers in cell and developmental biology · 2021
    Article
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Fang JinDepartment of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America.
Masakazu Hamada
Liviu Malureanu
Karthik B Jeganathan
Wei Zhou
Dean E Morbeck
Jan M van Deursen
Mayo Clinic · US

Funding

BUBRI in Normal and Neoplastic GrowthR01CA096985 · NCI · MAYO CLINIC ROCHESTER · PI BAKER, DARREN · 2002 to 2022
$6.2M
NCI NIH HHS CA96985NCI NIH HHS R01 CA096985Wellcome Trust
6 · The paper itself

Abstract

Chromosome missegregation in germ cells is an important cause of unexplained infertility, miscarriages, and congenital birth defects in humans. However, the molecular defects that lead to production of aneuploid gametes are largely unknown. Cdc20, the activating subunit of the anaphase-promoting complex/cyclosome (APC/C), initiates sister-chromatid separation by ordering the destruction of two key anaphase inhibitors, cyclin B1 and securin, at the transition from metaphase to anaphase. The physiological significance and full repertoire of functions of mammalian Cdc20 are unclear at present, mainly because of the essential nature of this protein in cell cycle progression. To bypass this problem we generated hypomorphic mice that express low amounts of Cdc20. These mice are healthy and have a normal lifespan, but females produce either no or very few offspring, despite normal folliculogenesis and fertilization rates. When mated with wild-type males, hypomorphic females yield nearly normal numbers of fertilized eggs, but as these embryos develop, they become malformed and rarely reach the blastocyst stage. In exploring the underlying mechanism, we uncover that the vast majority of these embryos have abnormal chromosome numbers, primarily due to chromosome lagging and chromosome misalignment during meiosis I in the oocyte. Furthermore, cyclin B1, cyclin A2, and securin are inefficiently degraded in metaphase I; and anaphase I onset is markedly delayed. These results demonstrate that the physiologically effective threshold level of Cdc20 is high for female meiosis I and identify Cdc20 hypomorphism as a mechanism for chromosome missegregation and formation of aneuploid gametes.

Indexed as

MeiosisAneuploidyAnimalsBlastocystCarrier ProteinsCdc20 ProteinsCell Cycle ProteinsChromosome SegregationChromosomes, MammalianCyclinsFemaleFertilityFertilizationGene DosageInfertility, FemaleMaleCarrier ProteinsCdc20 protein, mouseCdc20 ProteinsCell Cycle ProteinsCyclinsSecurin

Identifiers

PMID20941357
PMCPMC2947999
OpenAlexW2153467137

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.