{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T07:08:21Z","timestamp":1790838501921,"version":"4.1.0"},"reference-count":51,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2011,11,1]],"date-time":"2011-11-01T00:00:00Z","timestamp":1320105600000},"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":[[2011,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    During infection,\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Streptococcus pneumoniae<\/jats:named-content>\n                    exists mainly in sessile biofilms rather than in planktonic form, except during sepsis. The capacity to form biofilms is believed to be important for nasopharyngeal colonization as well as disease pathogenesis, but relatively little is known about the regulation of this process. Here, we investigated the effect of exogenous iron [Fe(III)] as well as the role of\n                    <jats:italic>luxS<\/jats:italic>\n                    (encoding S-ribosylhomocysteine lyase) on biofilm formation by\n                    <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. pneumoniae<\/jats:named-content>\n                    D39. Fe(III) strongly enhanced biofilm formation at concentrations of \u226550 \u03bcM, while Fe(III) chelation with deferoxamine was inhibitory. Importantly, Fe(III) also upregulated the expression of\n                    <jats:italic>luxS<\/jats:italic>\n                    in wild-type D39. A\n                    <jats:italic>luxS<\/jats:italic>\n                    -deficient mutant (D39\n                    <jats:italic>luxS<\/jats:italic>\n                    ) failed to form a biofilm, even with Fe(III) supplementation, whereas a derivative overexpressing\n                    <jats:italic>luxS<\/jats:italic>\n                    (D39\n                    <jats:italic>luxS<\/jats:italic>\n                    +) exhibited enhanced biofilm formation capacity and could form a biofilm without added Fe(III). D39\n                    <jats:italic>luxS<\/jats:italic>\n                    exhibited reduced expression of the major Fe(III) transporter PiuA, and the cellular [Fe(III)] was significantly lower than that in D39; in contrast, D39\n                    <jats:italic>luxS<\/jats:italic>\n                    + had a significantly higher cellular [Fe(III)] than the wild type. The release of extracellular DNA, which is an important component of the biofilm matrix, also was directly related to\n                    <jats:italic>luxS<\/jats:italic>\n                    expression. Similarly, genetic competence, as measured by transformation frequency as well as the expression of competence genes\n                    <jats:italic>comD<\/jats:italic>\n                    ,\n                    <jats:italic>comX<\/jats:italic>\n                    ,\n                    <jats:italic>comW<\/jats:italic>\n                    ,\n                    <jats:italic>cglA<\/jats:italic>\n                    , and\n                    <jats:italic>dltA<\/jats:italic>\n                    and the murein hydrolase\n                    <jats:italic>cbpD<\/jats:italic>\n                    , which is associated with fratricide-dependent DNA release, all were directly related to\n                    <jats:italic>luxS<\/jats:italic>\n                    expression levels and were further upregulated by Fe(III). Moreover, mutagenesis of\n                    <jats:italic>cbpD<\/jats:italic>\n                    blocked biofilm formation. We propose that competence, fratricide, and biofilm formation are closely linked in pneumococci, and that\n                    <jats:italic>luxS<\/jats:italic>\n                    is a central regulator of these processes. We also propose that the stimulatory effects of Fe(III) on all of these parameters are due to the upregulation of\n                    <jats:italic>luxS<\/jats:italic>\n                    expression, and that LuxS provides for a positive Fe(III)-dependent amplification loop by increasing iron uptake.\n                  <\/jats:p>","DOI":"10.1128\/iai.05644-11","type":"journal-article","created":{"date-parts":[[2011,8,29]],"date-time":"2011-08-29T20:56:23Z","timestamp":1314651383000},"page":"4550-4558","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":99,"title":["LuxS Mediates Iron-Dependent Biofilm Formation, Competence, and Fratricide in Streptococcus pneumoniae"],"prefix":"10.1128","volume":"79","author":[{"given":"Claudia","family":"Trappetti","sequence":"first","affiliation":[{"name":"Research Centre for Infectious Diseases, School of Molecular and Biomedical Science, University of Adelaide, South Australia 5005, 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