{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T14:53:34Z","timestamp":1790780014562,"version":"4.1.0"},"update-to":[{"DOI":"10.1371\/journal.ppat.1014469","type":"new_version","label":"New version","source":"publisher","updated":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T00:00:00Z","timestamp":1784851200000}}],"reference-count":55,"publisher":"Public Library of Science (PLoS)","issue":"7","license":[{"start":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T00:00:00Z","timestamp":1784505600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI146103"],"award-info":[{"award-number":["R01 AI146103"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI073289"],"award-info":[{"award-number":["R01 AI073289"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007699","name":"University of Georgia","doi-asserted-by":"crossref","award":["Distinguished Research Professorship"],"award-info":[{"award-number":["Distinguished Research Professorship"]}],"id":[{"id":"10.13039\/100007699","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":["www.plospathogens.org"],"crossmark-restriction":false},"short-container-title":["PLoS Pathog"],"abstract":"<jats:p>\n                    Biofilm formation by the fungus\n                    <jats:italic>Candida albicans<\/jats:italic>\n                    is a central virulence trait that enables colonization of implanted medical devices and mucosal surfaces. Biofilm formation reflects a complex regulatory network, and depends upon multiple master regulators that include transcription factors Efg1 and Ndt80. It is well established that\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394 and\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 single gene mutants are defective in biofilm formation. We report here that an\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 double mutant of reference strain SC5314 is able to form a robust biofilm in vitro and in vivo. We refer to the\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 biofilm as an emergent biofilm because this phenotype could not have been predicted from the phenotypes of\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394 or\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 single gene mutants. In four additional strain backgrounds,\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 mutants do not form biofilms, but in all strain backgrounds the\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 mutants can form filamentous cells, which are components of biofilms. Emergent biofilm formation is especially pronounced in YPD\u2009+\u2009FBS medium at 30\u00b0C, and RNA-seq under those conditions reveals altered expression in the\n                    <jats:italic>efg1<\/jats:italic>\n                    \u0394\/\u0394\n                    <jats:italic>ndt80<\/jats:italic>\n                    \u0394\/\u0394 double mutant of biofilm-related genes: upregulation of\n                    <jats:italic>BCR1, UME6,<\/jats:italic>\n                    and\n                    <jats:italic>HGC1<\/jats:italic>\n                    , and downregulation of\n                    <jats:italic>ALS3, BRG1,<\/jats:italic>\n                    and\n                    <jats:italic>HWP1.<\/jats:italic>\n                    These gene expression changes suggest that the emergent biofilm program is partially distinct from the conventional biofilm program. This inference is supported by functional analysis: emergent biofilm formation is independent of Brg1, Rob1, Tec1, and Wor3, all of which have positive roles in conventional biofilm formation. Emergent biofilm formation depends upon the hyphal cyclin Hgc1, the biofilm transcription factors Bcr1 and Ume6, and the Bcr1\/Ume6-activated adhesin gene\n                    <jats:italic>FLO9<\/jats:italic>\n                    . The seemingly simple emergent biofilm program may represent a primordial surface colonization strategy.\n                  <\/jats:p>","DOI":"10.1371\/journal.ppat.1014469","type":"journal-article","created":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T17:41:17Z","timestamp":1784569277000},"page":"e1014469","update-policy":"https:\/\/doi.org\/10.1371\/journal.ppat.corrections_policy","source":"Crossref","is-referenced-by-count":2,"title":["An emergent biofilm program from inactivation of Candida albicans master regulators Efg1 and Ndt80"],"prefix":"10.1371","volume":"22","author":[{"given":"Eunsoo","family":"Do","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Zarnowski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David 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