{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,14]],"date-time":"2026-09-14T22:27:10Z","timestamp":1789424830388,"version":"build-2803163510"},"reference-count":44,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T00:00:00Z","timestamp":1398902400000},"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":[[2014,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    <jats:named-content content-type=\"genus-species\">Burkholderia pseudomallei<\/jats:named-content>\n                    is a Gram-negative rod and the causative agent of melioidosis, an emerging infectious disease of tropical and subtropical areas worldwide.\n                    <jats:named-content content-type=\"genus-species\">B. pseudomallei<\/jats:named-content>\n                    harbors a remarkable number of virulence factors, including six type VI secretion systems (T6SS). Using our previously described plaque assay screening system, we identified a\n                    <jats:named-content content-type=\"genus-species\">B. pseudomallei<\/jats:named-content>\n                    transposon mutant defective in the\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    gene that showed reduced plaque formation. The\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    locus is encoded within T6SS cluster 1 (T6SS1), which is known to be involved in the pathogenesis of\n                    <jats:named-content content-type=\"genus-species\">B. pseudomallei<\/jats:named-content>\n                    in mammalian hosts. For further analysis, a\n                    <jats:named-content content-type=\"genus-species\">B. pseudomallei<\/jats:named-content>\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    deletion (\n                    <jats:italic>Bp<\/jats:italic>\n                    \u0394\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    ) mutant and complemented mutant strain were constructed.\n                    <jats:named-content content-type=\"genus-species\">B. pseudomallei<\/jats:named-content>\n                    lacking the\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    gene was highly attenuated in BALB\/c mice, whereas the\n                    <jats:italic>in vivo<\/jats:italic>\n                    virulence of the complemented mutant strain was fully restored to the wild-type level. The\n                    <jats:italic>Bp<\/jats:italic>\n                    \u0394\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    mutant showed impaired intracellular replication and formation of multinucleated giant cells in macrophages compared with wild-type bacteria, whereas the induction of actin tail formation within host cells was not affected. These observations resembled the phenotype of a mutant lacking\n                    <jats:italic>hcp1<\/jats:italic>\n                    , which is an integral component of the T6SS1 apparatus and is associated with full functionality of the T6SS1. Transcriptional expression of the T6SS components\n                    <jats:italic>vgrG<\/jats:italic>\n                    ,\n                    <jats:italic>tssA<\/jats:italic>\n                    , and\n                    <jats:italic>hcp1<\/jats:italic>\n                    , as well as the T6SS regulators\n                    <jats:italic>virAG<\/jats:italic>\n                    ,\n                    <jats:italic>bprC<\/jats:italic>\n                    , and\n                    <jats:italic>bsaN<\/jats:italic>\n                    , was not dependent on\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    expression. However, secretion of Hcp1 was not detectable in the absence of\n                    <jats:italic>BPSS1504<\/jats:italic>\n                    . Thus, BPSS1504 seems to serve as a T6SS component that affects Hcp1 secretion and is therefore involved in the integrity of the T6SS1 apparatus.\n                  <\/jats:p>","DOI":"10.1128\/iai.01544-14","type":"journal-article","created":{"date-parts":[[2014,3,4]],"date-time":"2014-03-04T23:44:48Z","timestamp":1393976688000},"page":"2006-2015","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":41,"title":["<i>BPSS1504<\/i>\n                    , a Cluster 1 Type VI Secretion Gene, Is Involved in Intracellular Survival and Virulence of Burkholderia pseudomallei"],"prefix":"10.1128","volume":"82","author":[{"given":"Verena","family":"Hopf","sequence":"first","affiliation":[{"name":"Friedrich Loeffler Institute of Medical Microbiology, University Medicine Greifswald, Greifswald, 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