Evidence map›Paper›PMID 25407023›Full record

ArticleNature communications2014

Diversification of bacterial genome content through distinct mechanisms over different timescales.

Nicholas J Croucher, Paul G Coupland, Abbie E Stevenson, Alanna Callendrello, Stephen D Bentley, William P Hanage

Abstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
–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

119 citing papers in PubMed, 1 synthesis or guideline pooled it.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Nicholas J Croucher1] Centre for Communicable Disease Dynamics, Harvard School of Public Health, 677 Huntington Avenue, Boston, Massachusetts 02115, USA [2] Department of Infectious Disease Epidemiology, St. Mary's Campus, Imperial College, London W2 1PG, UK.
Paul G CouplandThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.
Abbie E StevensonCentre for Communicable Disease Dynamics, Harvard School of Public Health, 677 Huntington Avenue, Boston, Massachusetts 02115, USA.
Alanna CallendrelloCentre for Communicable Disease Dynamics, Harvard School of Public Health, 677 Huntington Avenue, Boston, Massachusetts 02115, USA.
Stephen D BentleyThe Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SA, UK.
William P HanageCentre for Communicable Disease Dynamics, Harvard School of Public Health, 677 Huntington Avenue, Boston, Massachusetts 02115, USA.

Funding

Post-PCV pneumococcal population genetics and resistanceR01AI066304 · NIAID · HARVARD PILGRIM HEALTH CARE, INC. · PI FINKELSTEIN, JONATHAN A · 2006 to 2014
$6.4M
NIAID NIH HHS R01 AI066304NIAID NIH HHS R01AI066304Wellcome Trust 098051
6 · The paper itself

Abstract

Bacterial populations often consist of multiple co-circulating lineages. Determining how such population structures arise requires understanding what drives bacterial diversification. Using 616 systematically sampled genomes, we show that Streptococcus pneumoniae lineages are typically characterized by combinations of infrequently transferred stable genomic islands: those moving primarily through transformation, along with integrative and conjugative elements and phage-related chromosomal islands. The only lineage containing extensive unique sequence corresponds to a set of atypical unencapsulated isolates that may represent a distinct species. However, prophage content is highly variable even within lineages, suggesting frequent horizontal transmission that would necessitate rapidly diversifying anti-phage mechanisms to prevent these viruses sweeping through populations. Correspondingly, two loci encoding Type I restriction-modification systems able to change their specificity over short timescales through intragenomic recombination are ubiquitous across the collection. Hence short-term pneumococcal variation is characterized by movement of phage and intragenomic rearrangements, with the slower transfer of stable loci distinguishing lineages.

Indexed as

Genetic VariationGenome, BacterialGenomic IslandsDNA Restriction-Modification EnzymesProphagesStreptococcus pneumoniaeTime FactorsDNA Restriction-Modification Enzymes

Identifiers

PMID25407023
PMCPMC4263131

What OpenQuestion holds

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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.