{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T02:59:52Z","timestamp":1790909992943,"version":"4.1.0"},"reference-count":38,"publisher":"Microbiology Society","issue":"12","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,12,1]]},"abstract":"<jats:p>\n                  <jats:italic>Burkholderia pseudomallei<\/jats:italic> is the causative agent of melioidosis, a fatal human tropical disease. The non-specific DNA-binding protein DpsA plays a key role in protecting <jats:italic>B. pseudomallei<\/jats:italic> from oxidative stress mediated, for example, by organic hydroperoxides. The regulation of <jats:italic>dpsA<\/jats:italic> expression is poorly understood but one possibility is that it is regulated in a cell population density-dependent manner via <jats:italic>N<\/jats:italic>-acylhomoserine lactone (AHL)-dependent quorum sensing (QS) since a <jats:italic>lux<\/jats:italic>-box motif has been located within the <jats:italic>dpsA<\/jats:italic> promoter region. Using liquid chromatography and tandem mass spectrometry, it was first established that <jats:italic>B. pseudomallei<\/jats:italic> strain PP844 synthesizes AHLs. These were identified as <jats:italic>N<\/jats:italic>-octanoylhomoserine lactone (C8-HSL), <jats:italic>N<\/jats:italic>-(3-oxooctanoyl)homoserine lactone (3-oxo-C8-HSL), <jats:italic>N<\/jats:italic>-(3-hydroxyoctanoyl)-homoserine lactone (3-hydroxy-C8-HSL), <jats:italic>N<\/jats:italic>-decanoylhomoserine lactone (C10-HSL), <jats:italic>N<\/jats:italic>-(3-hydroxydecanoyl) homoserine lactone (3-hydroxy-C10-HSL) and <jats:italic>N<\/jats:italic>-(3-hydroxydodecanoyl)homoserine lactone (3-hydroxy-C12-HSL). Mutation of the genes encoding the LuxI homologue BpsI or the LuxR homologue BpsR resulted in the loss of C8-HSL and 3-oxo-C8-HSL synthesis, demonstrating that BpsI was responsible for directing the synthesis of these AHLs only and that <jats:italic>bpsI<\/jats:italic> expression and hence C8-HSL and 3-oxo-C8-HSL production depends on BpsR. In <jats:italic>bpsI<\/jats:italic>, <jats:italic>bpsR<\/jats:italic> and <jats:italic>bpsIR<\/jats:italic> mutants, <jats:italic>dpsA<\/jats:italic> expression was substantially down-regulated. Furthermore, <jats:italic>dpsA<\/jats:italic> expression in <jats:italic>Escherichia coli<\/jats:italic> required both BpsR and C8-HSL. <jats:italic>bpsIR<\/jats:italic>-deficient mutants exhibited hypersensitivity to the organic hydroperoxide <jats:italic>tert<\/jats:italic>-butyl hydroperoxide by displaying a reduction in cell viability which was restored by provision of exogenous C8-HSL (<jats:italic>bpsI<\/jats:italic> mutant only), by complementation with the <jats:italic>bpsIR<\/jats:italic> genes or by overexpression of <jats:italic>dpsA<\/jats:italic>. These data indicate that in <jats:italic>B. pseudomallei<\/jats:italic>, QS regulates the response to oxidative stress at least in part via the BpsR\/C8-HSL-dependent regulation of DpsA.<\/jats:p>","DOI":"10.1099\/mic.0.29226-0","type":"journal-article","created":{"date-parts":[[2006,12,12]],"date-time":"2006-12-12T08:28:10Z","timestamp":1165912090000},"page":"3651-3659","source":"Crossref","is-referenced-by-count":56,"title":["Quorum sensing regulates dpsA and the oxidative stress response in Burkholderia pseudomallei"],"prefix":"10.1099","volume":"152","author":[{"given":"Putthapoom","family":"Lumjiaktase","sequence":"first","affiliation":[{"name":"Department of Pathology, Faculty of Medicine-Ramathibodi Hospital, Mahidol University, Rama VI Road, Bangkok 10400, Thailand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen P.","family":"Diggle","sequence":"additional","affiliation":[{"name":"Institute of Infection, Immunity and Inflammation, Centre for 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