Evidence map›Paper›PMID 21076080›Full record

ArticleBiology of reproduction2011

Zinc requirement during meiosis I-meiosis II transition in mouse oocytes is independent of the MOS-MAPK pathway.

Miranda L Bernhardt, Alison M Kim, Thomas V O'Halloran, Teresa K Woodruff

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 98 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The TRPV3 channel is a mediator of zinc influx and homeostasis in murine oocytes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. ZneLife · 2023
    Article
  8. Review
  9. Article
  10. ZnbioRxiv : the preprint server for biology · 2023
    Article
  11. The role of zinc in follicular development.Molecular biology reports · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Role of zinc in female reproduction.Biology of reproduction · 2021
    Review
  17. Review
  18. Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Miranda L BernhardtDepartment of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Alison M Kim
Thomas V O'Halloran
Teresa K Woodruff
Northwestern University · US

Funding

Transition Metal Regulation of Oocyte MaturationP01HD021921 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MAYO, KELLY E · 1987 to 2013
$18.5M
TRAINING PROGRAM IN REPRODUCTIVE BIOLOGYT32HD007068 · NICHD · NORTHWESTERN UNIVERSITY · PI LEVINE, JON E · 1985 to 2008
$2.3M
NICHD NIH HHS P01 HD-021921NICHD NIH HHS P01 HD021921NICHD NIH HHS T32 HD007068NICHD NIH HHS T32 HD-07068
6 · The paper itself

Abstract

Zinc is essential for many biological processes, including proper functioning of gametes. We recently reported that zinc levels rise by over 50% during oocyte maturation and that attenuation of zinc availability during this period could be achieved using the membrane-permeable heavy metal chelator N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN). This zinc insufficiency resulted in formation of large polar bodies, failure to establish metaphase II arrest, and impaired establishment of cortical polarity. As these phenotypes resemble those of MOS null oocytes, we examined the impact of zinc insufficiency on the MOS-MAPK pathway. Reduced levels of both MOS protein and phosphorylation of MAP2K1/2 are observed in zinc-insufficient oocytes; however, these differences appear only after completion of the first meiotic division. In addition, activation of the downstream effector of the MOS pathway, MAPK3/1, is not affected by zinc insufficiency, and reduced MOS levels are observed only with the presence of TPEN after the first polar body extrusion. These data are inconsistent with the hypothesis that reduced MOS mediates the observed phenotype. Finally, MOS overexpression does not rescue the phenotype of zinc-insufficient oocytes, confirming that the observed disruption of asymmetric division and spindle abnormalities cannot be attributed to impaired MOS signaling. Zinc-insufficient oocytes do not increase maturation promoting factor (MPF) activity following the first meiotic division, and increasing MPF activity through expression of nondegradable cyclin B1 partially rescues the ability of zinc-insufficient oocytes to enter metaphase II. Although we have shown that zinc has a novel role in the meiotic cell cycle, it is not mediated through the MOS-MAPK pathway.

Indexed as

Cell DivisionMeiosisActin Capping ProteinsAnimalsChromatinFemaleMAP Kinase Signaling SystemMesothelinMiceModels, BiologicalOocytesOogenesisPhosphorylationProto-Oncogene Proteins c-mosSignal TransductionZincActin Capping ProteinsChromatinMesothelinMsln protein, mouseProto-Oncogene Proteins c-mosZinc

Identifiers

PMID21076080
PMCPMC3043131
OpenAlexW2106903949

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.