Evidence map›Paper›PMID 35393552›Full record

ArticleHeredity2022

Gene conversion: a non-Mendelian process integral to meiotic recombination.

Alexander Lorenz, Samantha J Mpaulo

Open access · hybridAbstract read
In one paragraph

Article in Heredity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mapping Gene Drive Dynamics onto Mendelian Models.bioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. A pedigree-based map of crossovers and non-crossovers in aye-ayes (bioRxiv : the preprint server for biology · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Alexander LorenzInstitute of Medical Sciences (IMS), University of Aberdeen, Aberdeen, UK. a.lorenz@abdn.ac.uk.ORCID http://orcid.org/0000-0003-1925-3713
Samantha J MpauloInstitute of Medical Sciences (IMS), University of Aberdeen, Aberdeen, UK.
University of Aberdeen · GB

Funding

RCUK | Biotechnology and Biological Sciences Research Council (BBSRC) BB/M010996/1
6 · The paper itself

Abstract

Meiosis is undoubtedly the mechanism that underpins Mendelian genetics. Meiosis is a specialised, reductional cell division which generates haploid gametes (reproductive cells) carrying a single chromosome complement from diploid progenitor cells harbouring two chromosome sets. Through this process, the hereditary material is shuffled and distributed into haploid gametes such that upon fertilisation, when two haploid gametes fuse, diploidy is restored in the zygote. During meiosis the transient physical connection of two homologous chromosomes (one originally inherited from each parent) each consisting of two sister chromatids and their subsequent segregation into four meiotic products (gametes), is what enables genetic marker assortment forming the core of Mendelian laws. The initiating events of meiotic recombination are DNA double-strand breaks (DSBs) which need to be repaired in a certain way to enable the homologous chromosomes to find each other. This is achieved by DSB ends searching for homologous repair templates and invading them. Ultimately, the repair of meiotic DSBs by homologous recombination physically connects homologous chromosomes through crossovers. These physical connections provided by crossovers enable faithful chromosome segregation. That being said, the DSB repair mechanism integral to meiotic recombination also produces genetic transmission distortions which manifest as postmeiotic segregation events and gene conversions. These processes are non-reciprocal genetic exchanges and thus non-Mendelian.

Indexed as

Gene ConversionMeiosisChromosome SegregationDNA Breaks, Double-StrandedHomologous Recombination

Identifiers

PMID35393552
PMCPMC9273591
OpenAlexW4225475694

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.