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<pubDate>Sat, 26 Jul 2008 03:08:49 BST</pubDate>


	<title>CiteULike: Xavier Titball</title>
	<description>CiteULike: Xavier Titball</description>


	<link>http://www.citeulike.org/user/Xavier/author/Titball</link>
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<item rdf:about="http://www.citeulike.org/user/Xavier/article/2485535">
    <title>Genome sequencing shows that European isolates of Francisella tularensis subspecies tularensis are almost identical to US laboratory strain Schu S4.</title>
    <link>http://www.citeulike.org/user/Xavier/article/2485535</link>
    <description>&lt;i&gt;PLoS ONE, Vol. 2, No. 4. (2007)&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;BACKGROUND: Francisella tularensis causes tularaemia, a life-threatening zoonosis, and has potential as a biowarfare agent. F. tularensis subsp. tularensis, which causes the most severe form of tularaemia, is usually confined to North America. However, a handful of isolates from this subspecies was obtained in the 1980s from ticks and mites from Slovakia and Austria. Our aim was to uncover the origins of these enigmatic European isolates. METHODOLOGY/PRINCIPAL FINDINGS: We determined the complete genome sequence of FSC198, a European isolate of F. tularensis subsp. tularensis, by whole-genome shotgun sequencing and compared it to that of the North American laboratory strain Schu S4. Apparent differences between the two genomes were resolved by re-sequencing discrepant loci in both strains. We found that the genome of FSC198 is almost identical to that of Schu S4, with only eight SNPs and three VNTR differences between the two sequences. Sequencing of these loci in two other European isolates of F. tularensis subsp. tularensis confirmed that all three European isolates are also closely related to, but distinct from Schu S4. CONCLUSIONS/SIGNIFICANCE: The data presented here suggest that the Schu S4 laboratory strain is the most likely source of the European isolates of F. tularensis subsp. tularensis and indicate that anthropogenic activities, such as movement of strains or animal vectors, account for the presence of these isolates in Europe. Given the highly pathogenic nature of this subspecies, the possibility that it has become established wild in the heartland of Europe carries significant public health implications.</description>
    <dc:title>Genome sequencing shows that European isolates of Francisella tularensis subspecies tularensis are almost identical to US laboratory strain Schu S4.</dc:title>

    <dc:creator>RR Chaudhuri</dc:creator>
    <dc:creator>CP Ren</dc:creator>
    <dc:creator>L Desmond</dc:creator>
    <dc:creator>GA Vincent</dc:creator>
    <dc:creator>NJ Silman</dc:creator>
    <dc:creator>JK Brehm</dc:creator>
    <dc:creator>MJ Elmore</dc:creator>
    <dc:creator>MJ Hudson</dc:creator>
    <dc:creator>M Forsman</dc:creator>
    <dc:creator>KE Isherwood</dc:creator>
    <dc:creator>D Gurycová</dc:creator>
    <dc:creator>NP Minton</dc:creator>
    <dc:creator>RW Titball</dc:creator>
    <dc:creator>MJ Pallen</dc:creator>
    <dc:creator>R Vipond</dc:creator>
    <dc:identifier>doi:10.1371/journal.pone.0000352</dc:identifier>
    <dc:source>PLoS ONE, Vol. 2, No. 4. (2007)</dc:source>
    <dc:date>2008-03-07T16:30:09-00:00</dc:date>
    <prism:publicationYear>2007</prism:publicationYear>
    <prism:publicationName>PLoS ONE</prism:publicationName>
    <prism:issn>1932-6203</prism:issn>
    <prism:volume>2</prism:volume>
    <prism:number>4</prism:number>
    <prism:category>frank</prism:category>
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<item rdf:about="http://www.citeulike.org/user/Xavier/article/93312">
    <title>The complete genome sequence of Francisella tularensis, the causative agent of tularemia.</title>
    <link>http://www.citeulike.org/user/Xavier/article/93312</link>
    <description>&lt;i&gt;Nat Genet, Vol. 37, No. 2. (February 2005), pp. 153-159.&lt;/i&gt;&lt;br /&gt;&lt;br /&gt;Francisella tularensis is one of the most infectious human pathogens known. In the past, both the former Soviet Union and the US had programs to develop weapons containing the bacterium. We report the complete genome sequence of a highly virulent isolate of F. tularensis (1,892,819 bp). The sequence uncovers previously uncharacterized genes encoding type IV pili, a surface polysaccharide and iron-acquisition systems. Several virulence-associated genes were located in a putative pathogenicity island, which was duplicated in the genome. More than 10% of the putative coding sequences contained insertion-deletion or substitution mutations and seemed to be deteriorating. The genome is rich in IS elements, including IS630 Tc-1 mariner family transposons, which are not expected in a prokaryote. We used a computational method for predicting metabolic pathways and found an unexpectedly high proportion of disrupted pathways, explaining the fastidious nutritional requirements of the bacterium. The loss of biosynthetic pathways indicates that F. tularensis is an obligate host-dependent bacterium in its natural life cycle. Our results have implications for our understanding of how highly virulent human pathogens evolve and will expedite strategies to combat them.</description>
    <dc:title>The complete genome sequence of Francisella tularensis, the causative agent of tularemia.</dc:title>

    <dc:creator>P Larsson</dc:creator>
    <dc:creator>PC Oyston</dc:creator>
    <dc:creator>P Chain</dc:creator>
    <dc:creator>MC Chu</dc:creator>
    <dc:creator>M Duffield</dc:creator>
    <dc:creator>HH Fuxelius</dc:creator>
    <dc:creator>E Garcia</dc:creator>
    <dc:creator>G Hälltorp</dc:creator>
    <dc:creator>D Johansson</dc:creator>
    <dc:creator>KE Isherwood</dc:creator>
    <dc:creator>PD Karp</dc:creator>
    <dc:creator>E Larsson</dc:creator>
    <dc:creator>Y Liu</dc:creator>
    <dc:creator>S Michell</dc:creator>
    <dc:creator>J Prior</dc:creator>
    <dc:creator>R Prior</dc:creator>
    <dc:creator>S Malfatti</dc:creator>
    <dc:creator>A Sjöstedt</dc:creator>
    <dc:creator>K Svensson</dc:creator>
    <dc:creator>N Thompson</dc:creator>
    <dc:creator>L Vergez</dc:creator>
    <dc:creator>JK Wagg</dc:creator>
    <dc:creator>BW Wren</dc:creator>
    <dc:creator>LE Lindler</dc:creator>
    <dc:creator>SG Andersson</dc:creator>
    <dc:creator>M Forsman</dc:creator>
    <dc:creator>RW Titball</dc:creator>
    <dc:identifier>doi:10.1038/ng1499</dc:identifier>
    <dc:source>Nat Genet, Vol. 37, No. 2. (February 2005), pp. 153-159.</dc:source>
    <dc:date>2005-02-11T16:10:31-00:00</dc:date>
    <prism:publicationYear>2005</prism:publicationYear>
    <prism:publicationName>Nat Genet</prism:publicationName>
    <prism:issn>1061-4036</prism:issn>
    <prism:volume>37</prism:volume>
    <prism:number>2</prism:number>
    <prism:startingPage>153</prism:startingPage>
    <prism:endingPage>159</prism:endingPage>
    <prism:category>frank</prism:category>
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