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

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Fältnamn	Indikatorer	Metadata
000		05301naa a2200901 4500
001		oai:DiVA.org:umu-23397
003		SwePub
008		090613s2007 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-233972 URI
024	7	a https://doi.org/10.1186/gb-2007-8-6-r1022 DOI
040		a (SwePub)umu
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Rohmer, Laurence4 aut
245	1 0	a Comparison of Francisella tularensis genomes reveals evolutionary events associated with the emergence of human pathogenic strains
264	1	b BioMed Central,c 2007
338		a electronic2 rdacarrier
520		a BACKGROUND: Francisella 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. RESULTS: Comparison 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. CONCLUSION: The 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.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Mikrobiologi inom det medicinska området0 (SwePub)301092 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Microbiology in the medical area0 (SwePub)301092 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Infektionsmedicin0 (SwePub)302092 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Infectious Medicine0 (SwePub)302092 hsv//eng
653		a Alleles
653		a Bacterial Typing Techniques
653		a Cluster Analysis
653		a DNA Fingerprinting
653		a DNA; Bacterial/analysis/chemistry/isolation & purification
653		a Epidemiology; Molecular/*methods
653		a Francisella tularensis/classification/genetics/isolation & purification
653		a Genotype
653		a Minisatellite Repeats
653		a Molecular Sequence Data
653		a Phylogeny
653		a Sequence Analysis; DNA
653		a Variation (Genetics)/genetics
700	1	a Fong, Christine4 aut
700	1	a Abmayr, Simone4 aut
700	1	a Wasnick, Michael4 aut
700	1	a Larson Freeman, Theodore J4 aut
700	1	a Radey, Matthew4 aut
700	1	a Guina, Tina4 aut
700	1	a Svensson, Kerstinu Umeå universitet,Infektionssjukdomar4 aut0 (Swepub:umu)kensvn99
700	1	a Hayden, Hillary S4 aut
700	1	a Jacobs, Michael4 aut
700	1	a Gallagher, Larry A4 aut
700	1	a Manoil, Colin4 aut
700	1	a Ernst, Robert K4 aut
700	1	a Drees, Becky4 aut
700	1	a Buckley, Danielle4 aut
700	1	a Haugen, Eric4 aut
700	1	a Bovee, Donald4 aut
700	1	a Zhou, Yang4 aut
700	1	a Chang, Jean4 aut
700	1	a Levy, Ruth4 aut
700	1	a Lim, Regina4 aut
700	1	a Gillett, Will4 aut
700	1	a Guenthener, Don4 aut
700	1	a Kang, Allison4 aut
700	1	a Shaffer, Scott A4 aut
700	1	a Taylor, Greg4 aut
700	1	a Chen, Jinzhi4 aut
700	1	a Gallis, Byron4 aut
700	1	a D'Argenio, David A4 aut
700	1	a Forsman, Matsu Umeå universitet,Institutionen för molekylärbiologi (Medicinska fakulteten)4 aut
700	1	a Olson, Maynard V4 aut
700	1	a Goodlett, David R4 aut
700	1	a Kaul, Rajinder4 aut
700	1	a Miller, Samuel I4 aut
700	1	a Brittnacher, Mitchell J4 aut
710	2	a Umeå universitetb Infektionssjukdomar4 org
773	0	t Genome Biologyd : BioMed Centralg 8:6q 8:6x 1465-6906x 1474-760X
856	4	u https://doi.org/10.1186/gb-2007-8-6-r102y Fulltext
856	4	u https://umu.diva-portal.org/smash/get/diva2:223655/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
856	4	u https://genomebiology.biomedcentral.com/track/pdf/10.1186/gb-2007-8-6-r102
856	4 8	u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-23397
856	4 8	u https://doi.org/10.1186/gb-2007-8-6-r102

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