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dc.contributor.authorPollard, Dominic J
dc.contributor.authorYoung, Joanna C
dc.contributor.authorCovarelli, Valentina
dc.contributor.authorHerrera-Leon, Silvia 
dc.contributor.authorConnor, Thomas R
dc.contributor.authorFookes, Maria
dc.contributor.authorWalker, Danielle
dc.contributor.authorEcheita, Aurora 
dc.contributor.authorThomson, Nicholas R
dc.contributor.authorBerger, Cedric N
dc.contributor.authorFrankel, Gad
dc.identifier.citationInfect Immun . 2016 Nov 18;84(12):3618-3628.es_ES
dc.description.abstractSalmonella species utilize type III secretion systems (T3SSs) to translocate effectors into the cytosol of mammalian host cells, subverting cell signaling and facilitating the onset of gastroenteritis. In this study, we compared a draft genome assembly of Salmonella enterica subsp. salamae strain 3588/07 against the genomes of S. enterica subsp. enterica serovar Typhimurium strain LT2 and Salmonella bongori strain 12419. S. enterica subsp. salamae encodes the Salmonella pathogenicity island 1 (SPI-1), SPI-2, and the locus of enterocyte effacement (LEE) T3SSs. Though several key S Typhimurium effector genes are missing (e.g., avrA, sopB, and sseL), S. enterica subsp. salamae invades HeLa cells and contains homologues of S. bongori sboK and sboC, which we named seoC SboC and SeoC are homologues of EspJ from enteropathogenic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively), which inhibit Src kinase-dependent phagocytosis by ADP-ribosylation. By screening 73 clinical and environmental Salmonella isolates, we identified EspJ homologues in S. bongori, S. enterica subsp. salamae, and Salmonella enterica subsp. arizonae The β-lactamase TEM-1 reporter system showed that SeoC is translocated by the SPI-1 T3SS. All the Salmonella SeoC/SboC homologues ADP-ribosylate Src E310 in vitro Ectopic expression of SeoC/SboC inhibited phagocytosis of IgG-opsonized beads into Cos-7 cells stably expressing green fluorescent protein (GFP)-FcγRIIa. Concurrently, S. enterica subsp. salamae infection of J774.A1 macrophages inhibited phagocytosis of beads, in a seoC-dependent manner. These results show that S. bongori, S. enterica subsp. salamae, and S. enterica subsp. arizonae share features of the infection strategy of extracellular pathogens EPEC and EHEC and shed light on the complexities of the T3SS effector repertoires of Enterobacteriaceae.es_ES
dc.description.sponsorshipWTSI authors are supported by Wellcome Trust grant number 098051.es_ES
dc.publisherAmerican Society for Microbiology (ASM) es_ES
dc.subject.meshGenome, Bacterial es_ES
dc.subject.meshAmino Acid Sequence es_ES
dc.subject.meshAnimals es_ES
dc.subject.meshBacterial Proteins es_ES
dc.subject.meshCOS Cells es_ES
dc.subject.meshChlorocebus aethiops es_ES
dc.subject.meshGene Expression Regulation, Bacterial es_ES
dc.subject.meshHeLa Cells es_ES
dc.subject.meshHumans es_ES
dc.subject.meshPrevalence es_ES
dc.subject.meshReceptors, IgG es_ES
dc.subject.meshSalmonella enterica es_ES
dc.subject.meshType III Secretion Systems es_ES
dc.titleThe Type III Secretion System Effector SeoC of Salmonella enterica subsp. salamae and S. enterica subsp. arizonae ADP-Ribosylates Src and Inhibits Opsonophagocytosis.es_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.contributor.funderWellcome Trust 
dc.identifier.journalInfection and immunityes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.rights.accessRightsopen accesses_ES

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