• Media type: E-Article
  • Title: The Legionella pneumophila IcmS–LvgA protein complex is important for Dot/Icm‐dependent intracellular growth
  • Contributor: Vincent, Carr D.; Vogel, Joseph P.
  • imprint: Wiley, 2006
  • Published in: Molecular Microbiology
  • Language: English
  • DOI: 10.1111/j.1365-2958.2006.05243.x
  • ISSN: 0950-382X; 1365-2958
  • Origination:
  • Footnote:
  • Description: <jats:title>Summary</jats:title><jats:p>Many bacterial pathogens require a functional type IV secretion system (T4SS) for virulence. <jats:italic>Legionella pneumophila</jats:italic>, the causative agent of Legionnaires' disease, employs the Dot/Icm T4SS to inject a large number of protein substrates into its host, thereby altering phagosome trafficking. The <jats:italic>L. pneumophila</jats:italic> T4SS substrate SdeA has been shown to require the accessory factor IcmS for its export. IcmS, defined as a type IV adaptor, exists as a heterodimer with IcmW and this complex functions in a manner similar to a type III secretion chaperone. Here we report an interaction between IcmS and the previously identified virulence factor LvgA. Similar to the <jats:italic>icmS</jats:italic> mutant, the <jats:italic>lvgA</jats:italic> mutant appears to assemble a fully functional Dot/Icm complex. Both LvgA and IcmS are small, acidic proteins localized to the cytoplasm and are not exported by the Dot/Icm system, suggesting they form a novel type IV adaptor complex. Inactivation of <jats:italic>lvgA</jats:italic> causes a minimal defect in growth in the human monocytic cell line U937 and the environmental host <jats:italic>Acanthamoeba castellanii</jats:italic>. However, the <jats:italic>lvgA</jats:italic> mutant was severely attenuated for intracellular growth of <jats:italic>L. pneumophila</jats:italic> in mouse macrophages, suggesting LvgA may be a critical factor that confers host specificity.</jats:p>
  • Access State: Open Access