Evidence map›Paper›PMID 19763179›Full record

ArticlePLoS genetics2009

Meiotic recombination in human oocytes.

Edith Y Cheng, Patricia A Hunt, Theresa A Naluai-Cecchini, Corrine L Fligner, Victor Y Fujimoto, Tanya L Pasternack, Jackie M Schwartz, Jody E Steinauer, Tracey J Woodruff, Sheila M Cherry and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2009. 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
13.4field-weighted citation impact, top 1% 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, 112 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Human acrocentric chromosome short armbioRxiv : the preprint server for biology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Failure to recombine is a common feature of human oogenesis.American journal of human genetics · 2021
    Article
  17. Article
  18. Crossover Interference, Crossover Maturation, and Human Aneuploidy.BioEssays : news and reviews in molecular, cellular and developmental biology · 2019
    Review
  19. Article
  20. Shugoshin protects centromere pairing and promotes segregation of nonexchange partner chromosomes in meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2019
    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

14 authors at 4 institutions in 1 country.

Edith Y ChengDepartment of Obstetrics and Gynecology, University of Washington, Seattle, Washington, United States of America.
Patricia A Hunt
Theresa A Naluai-Cecchini
Corrine L Fligner
Victor Y Fujimoto
Tanya L Pasternack
Jackie M Schwartz
Jody E Steinauer
Tracey J Woodruff
Sheila M Cherry
Terah A Hansen
Rhea U Vallente
Karl W Broman
Terry J Hassold
University of California, San Francisco · USWashington State University · USUniversity of Washington · USUniversity of Wisconsin–Madison · US

Funding

TERTIARY STRUCTURES OF ACTIVIN AND ACTIVIN RECEPTORSP01HD013527 · NICHD · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI VALE, WYLIE W. · 1985 to 2008
$10.9M
A Program of Research in Population CytogeneticsR37HD021341 · NICHD · WASHINGTON STATE UNIVERSITY · PI HASSOLD, TERRY J · 2010 to 2019
$5.8M
A PROGRAM OF RESEARCH IN POPULATION CYTOGENETICSR01HD021341 · NICHD · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI HASSOLD, TERRY J · 1985 to 2009
$5.7M
Meiotic Studies of Chemicals With Estrogenic ActivityR01ES013527 · NIEHS · WASHINGTON STATE UNIVERSITY · PI HUNT, PATRICIA · 2005 to 2014
$4.5M
Project 2: Assessing the Effects on BPA Exposure on Early Human DevelopmentP20ES018135 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI WOODRUFF, TRACEY J. · 2010 to 2012
$617k
NICHD NIH HHS HD13527NICHD NIH HHS HD21341NICHD NIH HHS P01 HD013527NICHD NIH HHS R01 HD021341NICHD NIH HHS R37 HD021341NIEHS NIH HHS P20 ES018135NIEHS NIH HHS R01 ES013527
6 · The paper itself

Abstract

Studies of human trisomies indicate a remarkable relationship between abnormal meiotic recombination and subsequent nondisjunction at maternal meiosis I or II. Specifically, failure to recombine or recombination events located either too near to or too far from the centromere have been linked to the origin of human trisomies. It should be possible to identify these abnormal crossover configurations by using immunofluorescence methodology to directly examine the meiotic recombination process in the human female. Accordingly, we initiated studies of crossover-associated proteins (e.g., MLH1) in human fetal oocytes to analyze their number and distribution on nondisjunction-prone human chromosomes and, more generally, to characterize genome-wide levels of recombination in the human female. Our analyses indicate that the number of MLH1 foci is lower than predicted from genetic linkage analysis, but its localization pattern conforms to that expected for a crossover-associated protein. In studies of individual chromosomes, our observations provide evidence for the presence of "vulnerable" crossover configurations in the fetal oocyte, consistent with the idea that these are subsequently translated into nondisjunctional events in the adult oocyte.

Indexed as

Recombination, GeneticAdaptor Proteins, Signal TransducingAdolescentAdultChromosomes, HumanConfidence IntervalsFemaleFetusGenome, HumanHumansMeiosisMutL Protein Homolog 1Nuclear ProteinsOocytesProtein TransportSister Chromatid ExchangeAdaptor Proteins, Signal TransducingMLH1 protein, humanMutL Protein Homolog 1Nuclear Proteins

Identifiers

PMID19763179
PMCPMC2735652
OpenAlexW2106208837

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.