Pseudomonas aeruginosa fimLregulates multiple virulence functions by intersecting with Vfr-modulated pathways.

Autor: Whitchurch, Cynthia B., Beatson, Scott A., Comolli, James C., Jakobsen, Thania, Sargent, Jennifer L., Bertrand, Jacob J., West, Joyce, Klausen, Mikkel, Waite, Leslie L., Kang, Pil Jung, Tolker-Nielsen, Tim, Mattick, John S., Engel, Joanne N.
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Zdroj: Molecular Microbiology; Mar2005, Vol. 55 Issue 5, p1357-1378, 22p
Abstrakt: Virulence ofPseudomonas aeruginosainvolves the co-ordinate expression of a range of factors including type IV pili (tfp), the type III secretion system (TTSS) and quorum sensing. Tfp are required for twitching motility, efficient biofilm formation, and for adhesion and type III secretion (TTS)-mediated damage to mammalian cells. We describe a novel gene (fimL) that is required for tfp biogenesis and function, for TTS and for normal biofilm development inP. aeruginosa. The predicted product offimLis homologous to the N-terminal domain of ChpA, except that its putative histidine and threonine phosphotransfer sites have been replaced with glutamine.fimLmutants resemblevfrmutants in many aspects including increased autolysis, reduced levels of surface-assembled tfp and diminished production of type III secreted effectors. Expression ofvfr in transcan complementfimLmutants.vfrtranscription and production is reduced infimLmutants whereas cAMP levels are unaffected. Deletion and insertion mutants offimLfrequently revert to wild-type phenotypes suggesting that an extragenic suppressor mutation is able to overcome the loss offimL.vfrtranscription and production, as well as cAMP levels, are elevated in these revertants, whilePseudomonasquinolone signal (PQS) production is reduced. These results suggest that the site(s) of spontaneous mutation is in a gene(s) which lies upstream ofvfrtranscription, cAMP, production, and PQS synthesis. Our studies indicate that Vfr and FimL are components of intersecting pathways that control twitching motility, TTSS and autolysis inP. aeruginosa. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index