Francisella requires dynamic type VI secretion system and ClpB to deliver effectors for phagosomal escape.

Détails

Ressource 1Télécharger: ncomms15853.pdf (1256.90 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_DD0E858F0323
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Francisella requires dynamic type VI secretion system and ClpB to deliver effectors for phagosomal escape.
Périodique
Nature Communications
Auteur(s)
Brodmann M., Dreier R.F., Broz P., Basler M.
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
2017
Peer-reviewed
Oui
Volume
8
Pages
15853
Langue
anglais
Résumé
Francisella tularensis is an intracellular pathogen that causes the fatal zoonotic disease tularaemia. Critical for its pathogenesis is the ability of the phagocytosed bacteria to escape into the cell cytosol. For this, the bacteria use a non-canonical type VI secretion system (T6SS) encoded on the Francisella pathogenicity island (FPI). Here we show that in F. novicida T6SS assembly initiates at the bacterial poles both in vitro and within infected macrophages. T6SS dynamics and function depends on the general purpose ClpB unfoldase, which specifically colocalizes with contracted sheaths and is required for their disassembly. T6SS assembly depends on iglF, iglG, iglI and iglJ, whereas pdpC, pdpD, pdpE and anmK are dispensable. Importantly, strains lacking pdpC and pdpD are unable to escape from phagosome, activate AIM2 inflammasome or cause disease in mice. This suggests that PdpC and PdpD are T6SS effectors involved in phagosome rupture.

Pubmed
Web of science
Open Access
Oui
Création de la notice
28/11/2017 14:48
Dernière modification de la notice
20/08/2019 17:01
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