The type IV pilin, PilA, is required for full virulence of <it>Francisella tularensis </it>subspecies <it>tularensis</it>
2010
Forslund Anna-Lena | Salomonsson Emelie | Golovliov Igor | Kuoppa Kerstin | Michell Stephen | Titball Richard | Oyston Petra | Noppa Laila | Sjöstedt Anders | Forsberg Åke
<p>Abstract</p> <p>Background</p> <p>All four <it>Francisella tularensis </it>subspecies possess gene clusters with potential to express type IV pili (Tfp). These clusters include putative pilin genes, as well as <it>pilB</it>, <it>pilC </it>and <it>pilQ</it>, required for secretion and assembly of Tfp. A hallmark of Tfp is the ability to retract the pilus upon surface contact, a property mediated by the ATPase PilT. Interestingly, out of the two major human pathogenic subspecies only the highly virulent type A strains have a functional <it>pilT </it>gene.</p> <p>Results</p> <p>In a previous study, we were able to show that one pilin gene, <it>pilA</it>, was essential for virulence of a type B strain in a mouse infection model. In this work we have examined the role of several Tfp genes in the virulence of the pathogenic type A strain SCHU S4. <it>pilA</it>, <it>pilC</it>, <it>pilQ</it>, and <it>pilT </it>were mutated by in-frame deletion mutagenesis. Interestingly, when mice were infected with a mixture of each mutant strain and the wild-type strain, the <it>pilA, pilC </it>and <it>pilQ </it>mutants were out-competed, while the <it>pilT </it>mutant was equally competitive as the wild-type.</p> <p>Conclusions</p> <p>This suggests that expression and surface localisation of PilA contribute to virulence in the highly virulent type A strain, while PilT was dispensable for virulence in the mouse infection model.</p>
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