Evidence map›Paper›PMID 29330348›Full record

ArticleGenetics2018

Weak Epistasis May Drive Adaptation in Recombining Bacteria.

Brian J Arnold, Michael U Gutmann, Yonatan H Grad, Samuel K Sheppard, Jukka Corander, Marc Lipsitch, William P Hanage

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
8.5field-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

34 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  12. Genetic Characterization of Carbapenem-ResistantAntibiotics (Basel, Switzerland) · 2023
    Article
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  15. Review
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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

7 authors at 4 institutions in 4 countries.

Brian J ArnoldCenter for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115 barnold@hsph.harvard.edu.
Michael U GutmannSchool of Informatics, University of Edinburgh, EH8 9AB, United Kingdom.
Yonatan H GradDepartment of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115.ORCID 0000-0001-5646-1314
Samuel K SheppardDepartment of Biology and Biochemistry, University of Bath, BA2 7AY, United Kingdom.
Jukka CoranderDepartment of Biostatistics, University of Oslo, Blindern, 0317, Norway.
Marc LipsitchCenter for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115.
William P HanageCenter for Communicable Disease Dynamics, Harvard T. H. Chan School of Public Health, Boston, Massachusetts 02115.
Harvard University · USUniversity of Bath · GBUniversity of Edinburgh · GBUniversity of Helsinki · FI

Funding

Understanding and controlling antibiotic resistanceU54GM088558 · NIGMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI LIPSITCH, MARC · 2009 to 2018
$26.4M
VACCINATION AND THE EVOLUTIONARY DYNAMICS OF PNEUMOCOCCIR01AI048935 · NIAID · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI LIPSITCH, MARC · 2001 to 2016
$8.8M
Ecological and genetic contributions to the spread of resistance in pneumococcusR01AI106786 · NIAID · HARVARD SCHOOL OF PUBLIC HEALTH · PI HANAGE, WILLIAM · 2013 to 2017
$3.1M
The role of fitness epistasis and gene network interactions in bacterial evolutionF32GM120839 · NIGMS · HARVARD SCHOOL OF PUBLIC HEALTH · PI ARNOLD, BRIAN JOHN · 2016 to 2018
$125k
NIAID NIH HHS R01 AI048935NIAID NIH HHS R01 AI106786NIGMS NIH HHS F32 GM120839NIGMS NIH HHS U54 GM088558
6 · The paper itself

Abstract

The impact of epistasis on the evolution of multi-locus traits depends on recombination. While sexually reproducing eukaryotes recombine so frequently that epistasis between polymorphisms is not considered to play a large role in short-term adaptation, many bacteria also recombine, some to the degree that their populations are described as "panmictic" or "freely recombining." However, whether this recombination is sufficient to limit the ability of selection to act on epistatic contributions to fitness is unknown. We quantify homologous recombination in five bacterial pathogens and use these parameter estimates in a multilocus model of bacterial evolution with additive and epistatic effects. We find that even for highly recombining species (

Indexed as

Epistasis, GeneticRecombination, GeneticAdaptation, BiologicalBacteriaLinkage DisequilibriumPolymorphism, Single NucleotideQuantitative Trait LociSelection, Geneticapproximate Bayesian computationbacteriaepistasishomologous recombinationmultilocus selection

Identifiers

PMID29330348
PMCPMC5844334
OpenAlexW2608079295

What OpenQuestion holds

Textmetadata
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.