Open Access Highly Accessed Research article

The type IV pilin, PilA, is required for full virulence of Francisella tularensis subspecies tularensis

Anna-Lena Forslund12, Emelie Näslund Salomonsson12, Igor Golovliov3, Kerstin Kuoppa1, Stephen Michell4, Richard Titball4, Petra Oyston5, Laila Noppa1, Anders Sjöstedt3 and Åke Forsberg12*

Author Affiliations

1 CBRN Defence and Security, FOI Swedish Defence Research Agency, 901 82 Umeå, Sweden

2 Umeå Centre for Microbial Research (UCMR) and Laboratory for Molecular Infection Medicine (MIMS), Sweden, Department of Molecular Biology, Umeå University, 901 87 Umeå, Sweden

3 Umeå Centre for Microbial Research (UCMR) and Laboratory for Molecular Infection Medicine (MIMS), Sweden, Department of Clinical Microbiology, Umeå University, 901 85 Umeå, Sweden

4 School of Biosciences, University of Exeter, Devon, EX4 4QD, UK

5 Defence Science and Technology Laboratory, Porton Down, Salisbury, Wiltshire SP4 OJQ, UK

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BMC Microbiology 2010, 10:227  doi:10.1186/1471-2180-10-227

Published: 26 August 2010



All four Francisella tularensis subspecies possess gene clusters with potential to express type IV pili (Tfp). These clusters include putative pilin genes, as well as pilB, pilC and pilQ, 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 pilT gene.


In a previous study, we were able to show that one pilin gene, pilA, 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. pilA, pilC, pilQ, and pilT 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 pilA, pilC and pilQ mutants were out-competed, while the pilT mutant was equally competitive as the wild-type.


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.