Interaction between the Type III Effector VopO and GEF-H1 Activates the RhoA-ROCK Pathway
Many bacterial pathogens manipulate the actin cytoskeleton of mammalian cells to establish pathogenesis via invasion, to evade killing by phagocytes, to disrupt a barrier function, and to induce inflammation caused by translocation type III secretion (T3S) effector proteins. We demonstrated that the T3S effector protein (VopO) of the enteric pathogen Vibrio parahaemolyticus induced robust actin stress fiber formation in infected host cells. Furthermore, this actin rearrangement induced barrier disruption in a colon epithelial cell line. Although many types of effector proteins have been reported, VopO does not share homology with previously reported effector proteins, and no putative functional motifs could be identified. Finally, we determined that the direct binding of VopO to a RhoA guanine nucleotide exchange factor (GEF) is a key step in the induction of stress fiber formation. These findings indicate that VopO plays a unique role in the pathogenicity of V. parahaemolyticus.
Vyšlo v časopise:
Interaction between the Type III Effector VopO and GEF-H1 Activates the RhoA-ROCK Pathway. PLoS Pathog 11(3): e32767. doi:10.1371/journal.ppat.1004694
Kategorie:
Research Article
prolekare.web.journal.doi_sk:
https://doi.org/10.1371/journal.ppat.1004694
Souhrn
Many bacterial pathogens manipulate the actin cytoskeleton of mammalian cells to establish pathogenesis via invasion, to evade killing by phagocytes, to disrupt a barrier function, and to induce inflammation caused by translocation type III secretion (T3S) effector proteins. We demonstrated that the T3S effector protein (VopO) of the enteric pathogen Vibrio parahaemolyticus induced robust actin stress fiber formation in infected host cells. Furthermore, this actin rearrangement induced barrier disruption in a colon epithelial cell line. Although many types of effector proteins have been reported, VopO does not share homology with previously reported effector proteins, and no putative functional motifs could be identified. Finally, we determined that the direct binding of VopO to a RhoA guanine nucleotide exchange factor (GEF) is a key step in the induction of stress fiber formation. These findings indicate that VopO plays a unique role in the pathogenicity of V. parahaemolyticus.
Zdroje
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Hygiena a epidemiológia Infekčné lekárstvo LaboratóriumČlánok vyšiel v časopise
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