{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T02:06:38Z","timestamp":1792721198924,"version":"4.5.0"},"reference-count":42,"publisher":"American Society for Microbiology","issue":"10","license":[{"start":{"date-parts":[[2015,10,1]],"date-time":"2015-10-01T00:00:00Z","timestamp":1443657600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,10]]},"abstract":"ABSTRACT<\/jats:title>\n \n Legionella<\/jats:named-content>\n organisms are environmental bacteria and accidental human pathogens that can cause severe pneumonia, termed Legionnaires' disease. These bacteria replicate within a pathogen-derived vacuole termed the\n Legionella<\/jats:named-content>\n -containing vacuole (LCV). Our understanding of the development and dynamics of this vacuole is based on extensive analysis of\n Legionella pneumophila<\/jats:named-content>\n . Here, we have characterized the\n Legionella longbeachae<\/jats:named-content>\n replicative vacuole (\n longbeachae<\/jats:named-content>\n -LCV) and demonstrated that, despite important genomic differences, key features of the replicative LCV are comparable to those of the LCV of\n L. pneumophila<\/jats:named-content>\n (\n pneumophila<\/jats:named-content>\n -LCV). We constructed a Dot\/Icm-deficient strain by deleting\n dotB<\/jats:italic>\n and demonstrated the inability of this mutant to replicate inside THP-1 cells.\n L. longbeachae<\/jats:named-content>\n does not enter THP-1 cells as efficiently as\n L. pneumophila<\/jats:named-content>\n , and this is reflected in the observation that translocation of BlaM-RalF\n LLO<\/jats:sub>\n (where RalF\n LLO<\/jats:sub>\n is the\n L. longbeachae<\/jats:named-content>\n homologue of RalF) into THP-1 cells by the\n L. longbeachae<\/jats:named-content>\n Dot\/Icm system is less efficient than that by\n L. pneumophila<\/jats:named-content>\n . This difference is negated in A549 cells where\n L. longbeachae<\/jats:named-content>\n and\n L. pneumophila<\/jats:named-content>\n infect with similar entry dynamics. A \u03b2-lactamase assay was employed to demonstrate the translocation of a novel family of proteins, the\n R<\/jats:underline>\n ab-\n l<\/jats:underline>\n ike\n e<\/jats:underline>\n ffector (Rle) proteins. Immunofluorescence analysis confirmed that these proteins enter the host cell during infection and display distinct subcellular localizations, with RleA and RleC present on the\n longbeachae<\/jats:named-content>\n -LCV. We observed that the host Rab GTPase, Rab1, and the v-SNARE Sec22b are also recruited to the\n longbeachae<\/jats:named-content>\n -LCV during the early stages of infection, coinciding with the LCV avoiding endocytic maturation. These studies further our understanding of the\n L. longbeachae<\/jats:named-content>\n replicative vacuole, highlighting phenotypic similarities to the vacuole of\n L. pneumophila<\/jats:named-content>\n as well as unique aspects of LCV biology.\n <\/jats:p>","DOI":"10.1128\/iai.00461-15","type":"journal-article","created":{"date-parts":[[2015,7,28]],"date-time":"2015-07-28T01:01:53Z","timestamp":1438045313000},"page":"4081-4092","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":25,"title":["Dot\/Icm Effector Translocation by Legionella longbeachae Creates a Replicative Vacuole Similar to That of Legionella pneumophila despite Translocation of Distinct Effector Repertoires"],"prefix":"10.1128","volume":"83","author":[{"given":"Rebecca E.","family":"Wood","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrice","family":"Newton","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleanor A.","family":"Latomanski","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9240-2001","authenticated-orcid":false,"given":"Hayley J.","family":"Newton","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Melbourne at the Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"E313","article-title":"Australia's notifiable disease status, 2011: annual report of the National Notifiable Diseases Surveillance System","volume":"37","author":"NNDSS Annual Report Writing Group","year":"2013","unstructured":"NNDSS Annual Report Writing Group. 2013. 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