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E-GEOD-51043

ABSTRACT: Global impact of Salmonella type III secretion effector SteA on host cells

OTHER RELATED OMICS DATASETS IN: PRJNA219735

PROVIDER: E-GEOD-51043 | ExpressionAtlas | 2025-01-24

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-51043-analysis-methods.tsv	Tabular
	E-GEOD-51043-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-51043-configuration.xml	Xml
	E-GEOD-51043-percentile-ranks.tsv	Tabular
	E-GEOD-51043.condensed-sdrf.tsv	Tabular

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Homo sapiens

Project description:Global impact of Salmonella type III secretion effector SteA on host cells

| PRJNA219735 | ENA

Expression data from RAW264.7 cells infected with wild-type vs srfJ mutant Salmonella enterica serovar Typhimurium

Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have infected murine RAW264.7 macrophages with two strains of Salmonella enterica serovar Typhimurium. The comparison between cells infected with the wild-type strain and cells infected with a srfJ mutant revealed a number of genes that are differentially expressed when SrfJ is present.

2023-05-17 | GSE215053 | GEO

Expression data from HeLa cells transfected with plasmid expressing Salmonella effector SrfJ or HeLa cells transfected with the empty vector

Project description:SrfJ is an effector of the type III secretion systems of the Gram-negative intracellular pathogen Salmonella enterica serovar Typhimurium. To study the effects of this effector on global gene expression in host cells, we have expressed SrfJ on human HeLa cells through transient transfection. The comparison with HeLa cells transfected with a plasmid not expressing SrfJ, revealed a number of genes that are differentially expressed when SrfJ is present.

2023-05-17 | GSE215051 | GEO

Salmonella activation of STAT3 signaling by SarA effector promotes intracellular replication and production of IL-10

Project description:Salmonella enterica is an important foodborne pathogen that utilizes secreted effector proteins to manipulate host pathways to facilitate survival and dissemination. Different S. enterica serovars cause disease syndromes ranging from self-limited gastroenteritis to typhoid fever and vary in their repertoire of effectors. We leveraged this natural diversity to identify stm2585, here designated sarA (Salmonella anti-inflammatory response activator), as a Salmonella effector secreted primary by the SPI-2 type III secretion system. SarA is necessary and sufficient to induce STAT3 phosphorylation and IL-10 production, contributing to intracellular replication in vitro and bacterial load at systemic sites in mice. These results demonstrate that Salmonella has evolved effector mechanisms for regulating a host anti-inflammatory signaling pathway important in infection, autoimmunity, and cancer.

2018-06-01 | GSE104354 | GEO

Salmonella effector SopB reorganizes cytoskeletal vimentin to maintain replication vacuoles for efficient infection

Project description:Subversion of the host cytoskeleton is a critical virulence mechanism used by a variety of intracellular bacterial pathogens during their infectious life cycles. Growing evidence suggests that the tactics employed by pathogens are surprisingly diverse. Using proteomic and biochemical methods, we demonstrate that the S. Tm type III effector protein SopB potently interacts specifically with host cell IFs vimentin. After host cell entry, Salmonella replicates in Salmonella containing vacuoles (SCVs), which accumulate a dense meshwork of vimentin through the Salmonella SPI-1 type III secretion effector SopB. We also demonstrate an important role for SopB-vimentin interaction, in the cellular responses including pro-inflammatory cytokine production induced by Salmonella. Vimentin interacts with the N-terminus of the S. Tm T3SS effector protein SopB. Vimentin and its interaction with SopB are dispensable for S. Tm invasion, but are required for stable formation of SCVs which are essential for bacteria replication. Moreover, SopB lacking of N-terminus cdc42-binding domain loses the interaction with vimentin, suggesting that the small GTPase is critical in SopB triggered vimentin recruitment to form integrative SCVs. These findings establish that SCVs integrity of the bacterium specifically requires intermediate filaments vimentin, which is a prerequisite for highly efficient S. Tm replication.

2023-03-11 | PXD028785 | Pride

4D-FastDIA quantitative phosphorylation modification omics analysis before and after expression of Salmonella effector SteC in RAW264.7 cell

Project description:The Salmonella effector SteC is the only protein kinase encoded by Salmonella pathogenicity island 2 that is secreted through the type III secretion system. SteC is known to trigger actin rearrangement via the phosphorylated MEK pathway, and our previous experiments demonstrated that the migration process of macrophages found during Salmonella infection is dependent on the rearrangement of the host cell actin backbone and the action of SteC.To further investigate the target of SteC in the host, we constructed a SteC-RAW264.7 cell line and performed phosphomics analysis using 4D-FastDIA to identify the direct substrates of SteC that trigger macrophage migration and lead to cytoskeletal rearrangement.

2024-02-22 | PXD042038 | Pride

Project description:Host Factors Controlling Type III Secretion Effector Injection

| PRJNA1125864 | ENA

A metabolomics analysis of gallbladder lipid droplet formation due to Salmonella infection

Project description:To cause disease, Salmonella enterica serovar Typhimurium requires two type-III secretion systems, encoded on Salmonella Pathogenicity Islands 1 and 2 (SPI-1 and -2). These secretion systems serve to deliver virulence proteins, termed effectors, into the host cell cytosol. While the importance of these effector proteins to promote colonization and replication within the host has been established, the specific roles of individual secreted effectors in the disease process are not well understood. In this study, we used an in vivo gallbladder epithelial cell infection model to study the function of the SPI-2-encoded effector, SseL. Deletion of the sseL gene resulted in bacterial filamentation and elongation and unusual localization of Salmonella within infected epithelial cells. Infection with the ΔsseL strain also caused dramatic changes in lipid metabolism and led to massive accumulation of lipid droplets in infected cells. Some of these changes were investigated through metabolomics of gallbladder tissue. This phenotype was directly attributed to the deubiquitinase activity of SseL, as a Salmonella strain carrying a single point mutation in the catalytic cysteine resulted in the same phenotype as the deletion mutant. Excessive buildup of lipids due to the absence of a functional sseL gene was also observed in S. Typhimurium-infected livers. These results demonstrate that SseL alters host lipid metabolism in infected epithelial cells by modifying ubiquitination patterns of cellular targets.

2011-08-23 | GSE27604 | GEO

identification of the endogenous insoluble host targets of the Salmonella effectors SSeK3

Project description:Strains of Salmonella utilise two distinct type three secretion systems to deliver effector proteins directly into host cells. The Salmonella effector SseK3 is a arginine glycosyltransferase that modify mammalian proteins with N-acetyl glucosamine (GlcNAc). Here, we used Arg-GlcNAc glycopeptide immunoprecipitation and mass spectrometry appraoch to identify host proteins GlcNAcylated by endogenous levels of SseK3 during Salmonella infection. Focusing on the insoluble proteome we demostrate multiple typically insoluble proteins are targetted by SseK3 during infections. Surpisingly unlike SseK1 and the EPEC homologue NleB1 which target death domain contain proteins SseK3 appears to modify a number of proteins lacking death domains. These results demostrate that under endogenous infection non-death domain containing proteins can be modified by Salmonella.

2020-07-28 | PXD015082 | Pride

DNA methylation profiling and analysis of differentially methylated regions (DMRs) of the Arabidopsis cells that received type-III effectors delivered by Xanthomonas campestris pv. Campestris (Xcc) bacterial mutants

Project description:Due to low numbers and poor accessibility of host cells that are targeted for effector delivery, the actual biological functions of most effectors remain elusive. Here, we developed a novel Isolation Nuclei TArgeted by Bacterial Effectors (INTABE) system, which facilitates selectively recovering nuclei of the cells in Arabidopsis thaliana plants that have received type-III effectors of pathogenic Xanthomonas bacteria. Using these nuclei as studying materials, we analysed changes in host gene expression and their correlation with changes in DNA methylation induced by Xanthomonas effector Outer Protein D (XopD).

2022-10-22 | E-MTAB-10281 | biostudies-arrayexpress

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