Evidence map›Paper›PMID 17550600›Full record

ArticleGenome biology2007

Comparison of Francisella tularensis genomes reveals evolutionary events associated with the emergence of human pathogenic strains.

Laurence Rohmer, Christine Fong, Simone Abmayr, Michael Wasnick, Theodore J Larson Freeman, Matthew Radey, Tina Guina, Kerstin Svensson, Hillary S Hayden, Michael Jacobs and 25 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in Genome biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers.

0numbers the graph read from it
0cells of the map it votes in
149citing papers in PubMed
11.8field-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

149 citing papers in PubMed, 252 citations in OpenAlex.

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  16. Whole Genome Sequencing: Applications in Clinical Bacteriology.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2024
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  18. The rLVS ΔHuman vaccines & immunotherapeutics · 2023
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89 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

35 authors at 3 institutions in 2 countries.

Laurence RohmerDepartment of Genome Sciences, University of Washington, Campus Box 357710, 1705 NE Pacific street Seattle, Washington 98195, USA. lrohmer@u.washington.edu
Christine Fong
Simone Abmayr
Michael Wasnick
Theodore J Larson Freeman
Matthew Radey
Tina Guina
Kerstin Svensson
Hillary S Hayden
Michael Jacobs
Larry A Gallagher
Colin Manoil
Robert K Ernst
Becky Drees
Danielle Buckley
Eric Haugen
Donald Bovee
Yang Zhou
Jean Chang
Ruth Levy
Regina Lim
Will Gillett
Don Guenthener
Allison Kang
Scott A Shaffer
Greg Taylor
Jinzhi Chen
Byron Gallis
David A D'Argenio
Mats Forsman
Maynard V Olson
David R Goodlett
Rajinder Kaul
Samuel I Miller
Mitchell J Brittnacher
University of Washington · USSwedish Defence Research Agency · SEUmeå University · SE

Funding

Variation in Human Innate ImmunityU54AI057141 · NIAID · UNIVERSITY OF WASHINGTON · PI COOKSON, BRAD T · 2003 to 2013
$102.3M
NIAID NIH HHS U54 AI057141PHS HHS U54AIO57141
6 · The paper itself

Abstract

backgroundFrancisella tularensis subspecies tularensis and holarctica are pathogenic to humans, whereas the two other subspecies, novicida and mediasiatica, rarely cause disease. To uncover the factors that allow subspecies tularensis and holarctica to be pathogenic to humans, we compared their genome sequences with the genome sequence of Francisella tularensis subspecies novicida U112, which is nonpathogenic to humans.

resultsComparison of the genomes of human pathogenic Francisella strains with the genome of U112 identifies genes specific to the human pathogenic strains and reveals pseudogenes that previously were unidentified. In addition, this analysis provides a coarse chronology of the evolutionary events that took place during the emergence of the human pathogenic strains. Genomic rearrangements at the level of insertion sequences (IS elements), point mutations, and small indels took place in the human pathogenic strains during and after differentiation from the nonpathogenic strain, resulting in gene inactivation.

conclusionThe chronology of events suggests a substantial role for genetic drift in the formation of pseudogenes in Francisella genomes. Mutations that occurred early in the evolution, however, might have been fixed in the population either because of evolutionary bottlenecks or because they were pathoadaptive (beneficial in the context of infection). Because the structure of Francisella genomes is similar to that of the genomes of other emerging or highly pathogenic bacteria, this evolutionary scenario may be shared by pathogens from other species.

Indexed as

DNA Transposable ElementsEvolution, MolecularFrancisella tularensisGenome, BacterialHumansMutationPseudogenesVirulenceDNA Transposable Elements

Identifiers

PMID17550600
PMCPMC2394750
OpenAlexW2102789902

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.