Evidence map›Paper›PMID 29440567›Full record

ArticleCold Spring Harbor symposia on quantitative biology2017

Cellular and Molecular Mechanisms of Centromere Drive.

Michael A Lampson, Ben E Black

Erratum issuedAbstract read
In one paragraph

Article in Cold Spring Harbor symposia on quantitative biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
–field-weighted citation impact
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

44 citing papers in PubMed.

  1. Article
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  5. Article
  6. Oocyte Kinetochores at the Nexus of Meiotic Drive and Segregation Fidelity.Advances in experimental medicine and biology · 2026
    Review
  7. Article
  8. CENP-A is diluted during bovine spermatogenesis and is maintained at internally positioned centromere clusters in mature bull sperm.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Marking dad's centromeres: maintaining CENP-A in sperm.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Meiotic drive of noncentromeric loci in mammalian meiosis II eggs.Current opinion in genetics & development · 2023
    Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Michael A LampsonDepartment of Biology, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Ben E BlackDepartment of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6059.

Funding

Cell Biological mechanisms of centromere driveR35GM122475 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI Michael Lampson · 2017 to 2026
$4.5M
Centromere Identity and FunctionR01GM082989 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BLACK, BEN E. · 2008 to 2018
$3.6M
NIGMS NIH HHS R01 GM082989NIGMS NIH HHS R35 GM122475
6 · The paper itself

Abstract

The asymmetric outcome of female meiosis I, whereby an entire set of chromosomes are discarded into a polar body, presents an opportunity for selfish genetic elements to cheat the process and disproportionately segregate to the egg. Centromeres, the chromosomal loci that connect to spindle microtubules, could potentially act as selfish elements and "drive" in meiosis. We review the current understanding of the genetic and epigenetic contributions to centromere identity and describe recent progress in a powerful model system to study centromere drive in mice. The progress includes mechanistic findings regarding two main requirements for a centromere to exploit the asymmetric outcome of female meiosis. The first is an asymmetry between centromeres of homologous chromosomes, and we found this is accomplished through massive changes in the abundance of the repetitive DNA underlying centromeric chromatin. The second requirement is an asymmetry in the meiotic spindle, which is achieved through signaling from the oocyte cortex that leads to asymmetry in a posttranslational modification of tubulin, tyrosination. Together, these two asymmetries culminate in the biased segregation of expanded centromeres to the egg, and we describe a mechanistic framework to understand this process.

Identifiers

PMID29440567
PMCPMC6041145

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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.