{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T02:21:41Z","timestamp":1790389301190,"version":"4.1.0"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2017,1,30]],"date-time":"2017-01-30T00:00:00Z","timestamp":1485734400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2017,2,15]],"date-time":"2017-02-15T00:00:00Z","timestamp":1487116800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100010269","name":"Wellcome","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000265","name":"RCUK | Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2017,2,15]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Strains of the various\n                    <jats:named-content content-type=\"genus-species\">Salmonella enterica<\/jats:named-content>\n                    serovars cause gastroenteritis or typhoid fever in humans, with virulence depending on the action of two type III secretion systems (\n                    <jats:named-content content-type=\"genus-species\">Salmonella<\/jats:named-content>\n                    pathogenicity island 1 [SPI-1] and SPI-2). SptP is a\n                    <jats:named-content content-type=\"genus-species\">Salmonella<\/jats:named-content>\n                    SPI-1 effector, involved in mediating recovery of the host cytoskeleton postinfection. SptP requires a chaperone, SicP, for stability and secretion. SptP has 94% identity between\n                    <jats:named-content content-type=\"genus-species\">S. enterica<\/jats:named-content>\n                    serovar Typhimurium and\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi; direct comparison of the protein sequences revealed that\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi SptP has numerous amino acid changes within its chaperone-binding domain. Subsequent comparison of \u0394\n                    <jats:italic>sptP S<\/jats:italic>\n                    . Typhi and\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium strains demonstrated that, unlike SptP in\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium, SptP in\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi was not involved in invasion or cytoskeletal recovery postinfection. Investigation of whether the observed amino acid changes within SptP of\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi affected its function revealed that\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi SptP was unable to complement\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium \u0394\n                    <jats:italic>sptP<\/jats:italic>\n                    due to an absence of secretion. We further demonstrated that while\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium SptP is stable intracellularly within\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi,\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi SptP is unstable, although stability could be recovered following replacement of the chaperone-binding domain with that of\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium. Direct assessment of the strength of the interaction between SptP and SicP of both serovars via bacterial two-hybrid analysis demonstrated that\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi SptP has a significantly weaker interaction with SicP than the equivalent proteins in\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium. Taken together, our results suggest that changes within the chaperone-binding domain of SptP in\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi hinder binding to its chaperone, resulting in instability, preventing translocation, and therefore restricting the intracellular activity of this effector.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>IMPORTANCE<\/jats:bold>\n                    Studies investigating\n                    <jats:named-content content-type=\"genus-species\">Salmonella<\/jats:named-content>\n                    pathogenesis typically rely on\n                    <jats:named-content content-type=\"genus-species\">Salmonella<\/jats:named-content>\n                    Typhimurium, even though\n                    <jats:named-content content-type=\"genus-species\">Salmonella<\/jats:named-content>\n                    Typhi causes the more severe disease in humans. As such, an understanding of\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhi pathogenesis is lacking. Differences within the type III secretion system effector SptP between typhoidal and nontyphoidal serovars led us to characterize this effector within\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi. Our results suggest that SptP is not translocated from typhoidal serovars, even though the loss of\n                    <jats:italic>sptP<\/jats:italic>\n                    results in virulence defects in\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium. Although SptP is just one effector, our results exemplify that the behavior of these serovars is significantly different and genes identified to be important for\n                    <jats:named-content content-type=\"genus-species\">S.<\/jats:named-content>\n                    Typhimurium virulence may not translate to\n                    <jats:italic>S<\/jats:italic>\n                    . Typhi.\n                  <\/jats:p>","DOI":"10.1128\/jb.00647-16","type":"journal-article","created":{"date-parts":[[2016,12,5]],"date-time":"2016-12-05T22:00:37Z","timestamp":1480975237000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":45,"title":["The Type III Secretion System Effector SptP of Salmonella enterica Serovar Typhi"],"prefix":"10.1128","volume":"199","author":[{"given":"Rebecca","family":"Johnson","sequence":"first","affiliation":[{"name":"MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Byrne","sequence":"additional","affiliation":[{"name":"MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cedric N.","family":"Berger","sequence":"additional","affiliation":[{"name":"MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Klemm","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie F.","family":"Crepin","sequence":"additional","affiliation":[{"name":"MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gordon","family":"Dougan","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gad","family":"Frankel","sequence":"additional","affiliation":[{"name":"MRC Centre for Molecular Bacteriology and Infection, Department of Life Sciences, Imperial College London, London, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.icb.7100007"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.mib.2008.12.001"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.058115-0"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.00066-12"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1286-4579(01)01495-2"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-6968.2010.01904.x"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1229224"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.183.15.4652-4658.2001"},{"key":"e_1_3_3_10_2","first-page":"177","article-title":"The virulence plasmids of Salmonella","volume":"2","author":"Rotger R","year":"1999","unstructured":"Rotger R Casadesus J . 1999. 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