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Translocation of a Vibrio cholerae Type VI Secretion Effector Requires Bacterial Endocytosis by Host Cells
被引:222
作者:
Ma, Amy T.
[1
]
McAuley, Steven
[2
]
Pukatzki, Stefan
[2
]
Mekalanos, John J.
[1
]
机构:
[1] Harvard Univ, Sch Med, Dept Microbiol & Mol Genet, Boston, MA 02115 USA
[2] Univ Alberta, Dept Med Microbiol & Immunol, Edmonton, AB T6G 2H7, Canada
基金:
美国国家卫生研究院;
关键词:
ENTEROAGGREGATIVE ESCHERICHIA-COLI;
COVALENT CROSS-LINKING;
RTX TOXIN;
EL-TOR;
PECTOBACTERIUM-ATROSEPTICUM;
BURKHOLDERIA-PSEUDOMALLEI;
PATHOGENICITY ISLAND;
COLONIZATION FACTOR;
EDWARDSIELLA-TARDA;
BETA-LACTAMASE;
D O I:
10.1016/j.chom.2009.02.005
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
The type VI secretion system (T6SS) is a virulence mechanism common to several Gram-negative pathogens. In Vibrio cholerae, VgrG-1 is required for T6SS-dependent secretion. VgrG-1 is also secreted by T6SS and displays a C-terminal actin crosslinking domain (ACID). Using a heterologous reporter enzyme in place of the ACD, we show that the effector and secretion functions of VgrG-1 are genetically dissociable with the ACID being dispensable for secretion but required for T6SS-dependent phenotypes. Furthermore, internalization of bacteria is required for ACD translocation into phagocytic target cells. Inhibiting bacterial uptake abolishes actin crosslinking, while improving intracellular survival enhances it. Otherwise resistant nonphagocytic cells become susceptible to T6SS-mediated actin crosslinking when engineered to take up bacteria. Our results support a model for translocation of VgrG C-terminal effector domains into target cell cytosol by a process that requires trafficking of bacterial cells into an endocytic compartment where translocation is triggered by an unknown signal.
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页码:234 / 243
页数:10
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