Evidence map›Paper›PMID 27633831›Full record

ArticleNature communications2016

Sequence element enrichment analysis to determine the genetic basis of bacterial phenotypes.

John A Lees, Minna Vehkala, Niko Välimäki, Simon R Harris, Claire Chewapreecha, Nicholas J Croucher, Pekka Marttinen, Mark R Davies, Andrew C Steer, Steven Y C Tong and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 2 pooled it
25.4field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 2 syntheses or guidelines pooled it, 223 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  12. Article
  13. Genome analysis of colistin-resistantFrontiers in microbiology · 2025
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Microbial genomics · 2024
    Article

64 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

14 authors at 8 institutions in 4 countries.

John A LeesPathogen Genomics, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.ORCID 0000-0001-5360-1254
Minna VehkalaDepartment of Mathematics and Statistics, University of Helsinki, Helsinki FI-00014, Finland.
Niko VälimäkiDepartment of Medical and Clinical Genetics, Genome-Scale Biology Research Program, University of Helsinki, Helsinki FI-00014, Finland.
Simon R HarrisPathogen Genomics, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Claire ChewapreechaDepartment of Medicine, University of Cambridge, Cambridge CB2 0SP, UK.
Nicholas J CroucherDepartment of Infectious Disease Epidemiology, Imperial College, London W2 1NY, UK.
Pekka MarttinenDepartment of Computer Science, Aalto University, Espoo FI-00076, Finland.
Mark R DaviesDepartment of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, Victoria 3010, Australia.
Andrew C SteerCentre for International Child Health, Department of Paediatrics, University of Melbourne, Melbourne, Victoria 3052, Australia.
Steven Y C TongMenzies School of Health Research, Darwin, Northern Territory 0811, Australia.
Antti HonkelaHelsinki Institute for Information Technology HIIT, Department of Computer Science, University of Helsinki, Helsinki FI-00014, Finland.ORCID 0000-0001-9193-8093
Julian ParkhillPathogen Genomics, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.ORCID 0000-0002-7069-5958
Stephen D BentleyPathogen Genomics, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Jukka CoranderPathogen Genomics, Wellcome Trust Sanger Institute, Cambridge CB10 1SA, UK.
Wellcome Sanger Institute · GBStatistics Finland · FIThe University of Melbourne · AUUniversity of Helsinki · FIHelsinki Institute for Information Technology · FIImperial College London · GBMenzies School of Health Research · AUUniversity of Cambridge · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Bacterial genomes vary extensively in terms of both gene content and gene sequence. This plasticity hampers the use of traditional SNP-based methods for identifying all genetic associations with phenotypic variation. Here we introduce a computationally scalable and widely applicable statistical method (SEER) for the identification of sequence elements that are significantly enriched in a phenotype of interest. SEER is applicable to tens of thousands of genomes by counting variable-length k-mers using a distributed string-mining algorithm. Robust options are provided for association analysis that also correct for the clonal population structure of bacteria. Using large collections of genomes of the major human pathogens Streptococcus pneumoniae and Streptococcus pyogenes, SEER identifies relevant previously characterized resistance determinants for several antibiotics and discovers potential novel factors related to the invasiveness of S. pyogenes. We thus demonstrate that our method can answer important biologically and medically relevant questions.

Indexed as

Computer SimulationDNA, BacterialGenome, BacterialGenome-Wide Association StudyModels, GeneticNucleic Acid Amplification TechniquesStreptococcus pneumoniaeStreptococcus pyogenesDNA, Bacterial

Identifiers

PMID27633831
PMCPMC5028413
OpenAlexW2949477823

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.