Evidence map›Paper›PMID 26161978›Full record

ArticlePloS one2015

Using Whole Genome Analysis to Examine Recombination across Diverse Sequence Types of Staphylococcus aureus.

Elizabeth M Driebe, Jason W Sahl, Chandler Roe, Jolene R Bowers, James M Schupp, John D Gillece, Erin Kelley, Lance B Price, Talima R Pearson, Crystal M Hepp and 7 more

Abstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Review
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  7. Biofilm forming multidrug resistantIranian journal of veterinary research · 2023
    Article
  8. Antimicrobial Resistance and Molecular Epidemiology ofPathogens (Basel, Switzerland) · 2022
    Article
  9. Article
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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

17 authors.

Elizabeth M DriebePathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Jason W SahlPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Chandler RoePathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Jolene R BowersPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
James M SchuppPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
John D GillecePathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Erin KelleyPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Lance B PricePathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Talima R PearsonCenter for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, Arizona, United States of America.
Crystal M HeppCenter for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, Arizona, United States of America.
Pius M BrzoskaThermo Fisher Scientific, South San Francisco, California, United States of America.
Craig A CummingsThermo Fisher Scientific, South San Francisco, California, United States of America.
Manohar R FurtadoThermo Fisher Scientific, South San Francisco, California, United States of America.
Paal S AndersenMicrobiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
Marc SteggerMicrobiology and Infection Control, Statens Serum Institut, Copenhagen, Denmark.
David M EngelthalerPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America.
Paul S KeimPathogen Genomics Division, The Translational Genomics Research Institute, Flagstaff, Arizona, United States of America; Center for Microbial Genetics and Genomics, Northern Arizona University, Flagstaff, Arizona, United States of America.

Funding

Molecular Antibiotic Resistance Arrays for clinical microbiology laboratoriesR01AI090782 · NIAID · TRANSLATIONAL GENOMICS RESEARCH INST · PI KEIM, PAUL STEPHEN · 2010 to 2014
$4.6M
Real-Time PCR Assays for Direct Detection of Sepsis and CAP PathogensU01AI066581 · NIAID · TRANSLATIONAL GENOMICS RESEARCH INST · PI KEIM, PAUL STEPHEN · 2005 to 2009
$3.0M
Rapid Emergence of Livestock-associated MRSA ST398: Host-adaptation & VirulenceR01AI101371 · NIAID · TRANSLATIONAL GENOMICS RESEARCH INST · PI PRICE, LANCE BRADLEY · 2013 to 2016
$1.6M
NIAID NIH HHS R01 AI090782NIAID NIH HHS R01AI090782NIAID NIH HHS R01 AI101371NIAID NIH HHS U01 AI066581
6 · The paper itself

Abstract

Staphylococcus aureus is an important clinical pathogen worldwide and understanding this organism's phylogeny and, in particular, the role of recombination, is important both to understand the overall spread of virulent lineages and to characterize outbreaks. To further elucidate the phylogeny of S. aureus, 35 diverse strains were sequenced using whole genome sequencing. In addition, 29 publicly available whole genome sequences were included to create a single nucleotide polymorphism (SNP)-based phylogenetic tree encompassing 11 distinct lineages. All strains of a particular sequence type fell into the same clade with clear groupings of the major clonal complexes of CC8, CC5, CC30, CC45 and CC1. Using a novel analysis method, we plotted the homoplasy density and SNP density across the whole genome and found evidence of recombination throughout the entire chromosome, but when we examined individual clonal lineages we found very little recombination. However, when we analyzed three branches of multiple lineages, we saw intermediate and differing levels of recombination between them. These data demonstrate that in S. aureus, recombination occurs across major lineages that subsequently expand in a clonal manner. Estimated mutation rates for the CC8 and CC5 lineages were different from each other. While the CC8 lineage rate was similar to previous studies, the CC5 lineage was 100-fold greater. Fifty known virulence genes were screened in all genomes in silico to determine their distribution across major clades. Thirty-three genes were present variably across clades, most of which were not constrained by ancestry, indicating horizontal gene transfer or gene loss.

Indexed as

Genetic VariationRecombination, GeneticBayes TheoremCluster AnalysisEvolution, MolecularGenes, BacterialGenome, BacterialGenotypeMutationMutation RatePhylogenyPolymorphism, Single NucleotideSequence Analysis, DNAStaphylococcus aureusVirulence

Identifiers

PMID26161978
PMCPMC4498916

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.