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Identified virulence factors of Salmonella: Toxin


SpvB  

Related genes: spvB;
Keywords: Toxin; Intracellular toxin; ADP-ribosyltransferase;
Structure features:
PDB accession: 2GWL.
Functions:
SpvB-mediated actin depolymerization is associated with an accumulation of cells in the G2/M phase, eventually resulting in apoptotic cell death.
Mechanism:
An ADP-ribosylating toxin that modifies actin directly and totally disrupt the cytoskeleton of the cell.
References:
Gulig PA, et al., 1993. Molecular analysis of spv virulence genes of the Salmonella virulence plasmids. Mol. Microbiol. 7(6):825-830.
Marshall DG, et al., 1999. A role for the leucine-responsive regulatory protein and integration host factor in the regulation of the Salmonella plasmid virulence (spv ) locus in Salmonella typhimurium. Mol. Microbiol. 34(1):134-145.
Libby SJ, et al., 2000. The Salmonella virulence plasmid spv genes are required for cytopathology in human monocyte-derived macrophages. Cell. Microbiol. 2(1):49-58.
Lesnick ML, et al., 2001. The Salmonella spvB virulence gene encodes an enzyme that ADP-ribosylates actin and destabilizes the cytoskeleton of eukaryotic cells. Mol. Microbiol. 39(6):1464-1470.
Matsui H, et al., 2001. Virulence plasmid-borne spvB and spvC genes can replace the 90-kilobase plasmid in conferring virulence to Salmonella enterica serovar Typhimurium in subcutaneously inoculated mice. J. Bacteriol. 183(15):4652-4658.
Gotoh H, et al., 2003. Extracellular secretion of the virulence plasmid-encoded ADP-ribosyltransferase SpvB in Salmonella. Microb. Pathog. 34(5):227-238.
Kurita A, et al., 2003. Intracellular expression of the Salmonella plasmid virulence protein, SpvB, causes apoptotic cell death in eukaryotic cells. Microb. Pathog. 35(1):43-48.


Typhoid toxin  

Related genes: cdtB; pltA; pltB;
Keywords: Toxin; Intracellular toxin; DNaseI; ADPRT;
Characteristics:
Classic cytolethal distending toxins (CDTs) are three component AB toxins, composed of CdtA, CdtB and CdtC. CdtA and CdtC mediate target cell binding and membrane translocation of CdtB, which then induces DNA damage, most probably through its nuclease activity.
In the case of S. typhi, however, genes encoding CdtA and CdtC are absent. CdtB from S. typhi is produced with the pertussis-like toxins PltA and PltB only inside the host cell and is then secreted from the infected Cell in a PltA/B-Dependent manner and acts then as a classical CDT from outside.
Typhoid toxin seemed to have evolved from the combination of the activities of two exotoxin ancestors, CDT and pertussis toxins.
Structure features:
A novel A2B5 architecture in which the A2 domain comprises one unit of CdtB and one unit of PltA and the B5 domain comprises five PltB subunits.
PDB accession: 4K6L.
Figures:
Typhoid toxin uses a unique intoxication mechanism (From: Simon NC, et al., 2014. Novel bacterial ADP-ribosylating toxins: structure and function. Nat Rev Microbiol 12(9):599-611.).


Functions:
CdtB involves chromatin disruption, which leads to G2/M-phase growth arrest of the target cell and ultimately cell death.
PltA ADP-ribosyltransferase activity targets an as-yet-unidentified protein.
References:
Haghjoo E, Galan JE, 2004. Salmonella typhi encodes a functional cytolethal distending toxin that is delivered into host cells by a bacterial-internalization pathway. Proc. Natl. Acad. Sci. USA. 101(13):4614-4619.
Spano S, et al., 2008. Delivery of a Salmonella Typhi exotoxin from a host intracellular compartment. Cell Host Microbe. 3(1):30-38.








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