Selective Inhibition of Type III Secretion Activated Signaling by the Salmonella Effector AvrA e1000595
Salmonella enterica utilizes a type III secretion system (TTSS) encoded in its pathogenicity island 1 to mediate its initial interactions with intestinal epithelial cells, which are characterized by the stimulation of actin cytoskeleton reorganization and a profound reprogramming of gene expression....
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Published in: | PLoS pathogens Vol. 5; no. 9 |
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01-09-2009
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Abstract | Salmonella enterica utilizes a type III secretion system (TTSS) encoded in its pathogenicity island 1 to mediate its initial interactions with intestinal epithelial cells, which are characterized by the stimulation of actin cytoskeleton reorganization and a profound reprogramming of gene expression. These responses result from the stimulation of Rho-family GTPases and downstream signaling pathways by specific effector proteins delivered by this TTSS. We show here that AvrA, an effector protein of this TTSS, specifically inhibits the Salmonella-induced activation of the JNK pathway through its interaction with MKK7, although it does not interfere with the bacterial infection-induced NF-κB activation. We also show that AvrA is phosphorylated at evolutionary conserved residues by a TTSS-effector-activated ERK pathway. This interplay between effector proteins delivered by the same TTSS highlights the remarkable complexity of these systems. |
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AbstractList | Salmonella enterica utilizes a type III secretion system (TTSS) encoded in its pathogenicity island 1 to mediate its initial interactions with intestinal epithelial cells, which are characterized by the stimulation of actin cytoskeleton reorganization and a profound reprogramming of gene expression. These responses result from the stimulation of Rho-family GTPases and downstream signaling pathways by specific effector proteins delivered by this TTSS. We show here that AvrA, an effector protein of this TTSS, specifically inhibits the Salmonella-induced activation of the JNK pathway through its interaction with MKK7, although it does not interfere with the bacterial infection-induced NF-κB activation. We also show that AvrA is phosphorylated at evolutionary conserved residues by a TTSS-effector-activated ERK pathway. This interplay between effector proteins delivered by the same TTSS highlights the remarkable complexity of these systems. |
Author | Du, Fangyong Galán, Jorge E |
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ContentType | Journal Article |
Copyright | 2009 Du, Galán. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Du F, Galán JE (2009) Selective Inhibition of Type III Secretion Activated Signaling by the Salmonella Effector AvrA. PLoS Pathog 5(9): e1000595. doi:10.1371/journal.ppat.1000595 |
Copyright_xml | – notice: 2009 Du, Galán. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Du F, Galán JE (2009) Selective Inhibition of Type III Secretion Activated Signaling by the Salmonella Effector AvrA. PLoS Pathog 5(9): e1000595. doi:10.1371/journal.ppat.1000595 |
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DOI | 10.1371/journal.ppat.1000595 |
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Snippet | Salmonella enterica utilizes a type III secretion system (TTSS) encoded in its pathogenicity island 1 to mediate its initial interactions with intestinal... |
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Title | Selective Inhibition of Type III Secretion Activated Signaling by the Salmonella Effector AvrA |
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