Evidence map›Paper›PMID 21220356›Full record

ArticleGenetics2011

The resolution of sexual antagonism by gene duplication.

Tim Connallon, Andrew G Clark

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 132 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. eLife · 2024
    Article
  8. On the resolution of sexual conflict over shared traits.Proceedings. Biological sciences · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Polygenic response of sex chromosomes to sexual antagonism.Evolution; international journal of organic evolution · 2024
    Article
  13. Sex-linked gene traffic underlies the acquisition of sexually dimorphic UV color vision inProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

9 more citing papers are in PubMed but not listed here.

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.

Tim ConnallonDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, New York 14853-2703, USA. tmc233@cornell.edu
Andrew G Clark
Cornell University · US

Funding

Molecular Evolution of Drosophila Y ChromosomeR01GM064590 · NIGMS · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI CARVALHO, ANTONIO BERNARDO, CLARK, ANDREW G · 2002 to 2012
$2.0M
NIGMS NIH HHS GM64590NIGMS NIH HHS R01 GM064590
6 · The paper itself

Abstract

Disruptive selection between males and females can generate sexual antagonism, where alleles improving fitness in one sex reduce fitness in the other. This type of genetic conflict arises because males and females carry nearly identical sets of genes: opposing selection, followed by genetic mixing during reproduction, generates a population genetic "tug-of-war" that constrains adaptation in either sex. Recent verbal models suggest that gene duplication and sex-specific cooption of paralogs might resolve sexual antagonism and facilitate evolutionary divergence between the sexes. However, this intuitive proximal solution for sexual dimorphism potentially belies a complex interaction between mutation, genetic drift, and positive selection during duplicate fixation and sex-specific paralog differentiation. The interaction of these processes--within the explicit context of duplication and sexual antagonism--has yet to be formally described by population genetics theory. Here, we develop and analyze models of gene duplication and sex-specific differentiation between paralogs. We show that sexual antagonism can favor the fixation and maintenance of gene duplicates, eventually leading to the evolution of sexually dimorphic genetic architectures for male and female traits. The timescale for these evolutionary transitions is sensitive to a suite of genetic and demographic variables, including allelic dominance, recombination, sex linkage, and population size. Interestingly, we find that female-beneficial duplicates preferentially accumulate on the X chromosome, whereas male-beneficial duplicates are biased toward autosomes, independent of the dominance parameters of sexually antagonistic alleles. Although this result differs from previous models of sexual antagonism, it is consistent with several findings from the empirical genomics literature.

Indexed as

Evolution, MolecularSexAllelesAnimalsFemaleGene DuplicationHumansMaleSelection, GeneticX Chromosome

Identifiers

PMID21220356
PMCPMC3063682
OpenAlexW2129461897

What OpenQuestion holds

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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.