{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T06:19:23Z","timestamp":1789193963358,"version":"build-2803163510"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:00:00Z","timestamp":1779408000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["R21 AI185250"],"award-info":[{"award-number":["R21 AI185250"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","award":["R01 DE026600"],"award-info":[{"award-number":["R01 DE026600"]}],"id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007699","name":"University of Georgia","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007699","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,7,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Candida albicans is an opportunistic fungal pathogen and a component of the human microbiome. C. albicans virulence traits include biofilm production, which is governed by a large transcriptional network. Mutations of some biofilm regulators cause the same severe biofilm-defective phenotype in multiple clinical isolates. Mutations of others, such as Wor3, Bcr1, Ndt80, and Ume6, have mild or variable phenotypes among clinical isolates. We hypothesized that Wor3 may share functions with another variable-phenotype biofilm regulator. This hypothesis predicts that a double mutant lacking Wor3 and the shared-function regulator will have a severe biofilm defect in all clinical isolates. We observed that a wor3\u0394\/\u0394 bcr1\u0394\/\u0394 double mutant has a severe biofilm defect in vitro in 5 strain backgrounds tested. It also has a severe oral biofilm defect in a mouse oropharyngeal candidiasis model in the SC5314 strain background. RNA-seq data indicate that 5 genes encoding cell surface\/secreted proteins are upregulated in wor3\u0394\/\u0394, bcr1\u0394\/\u0394, and wor3\u0394\/\u0394 bcr1\u0394\/\u0394 strains: CWH8, DAG7, JEN2, PGA6, and YWP1. Deletion mutations of CWH8, DAG7, PGA6, or YWP1 enable biofilm formation in vitro in an SC5314-derived wor3\u0394\/\u0394 bcr1\u0394\/\u0394 strain, and deletion of YWP1 enables biofilm formation in vitro in wor3\u0394\/\u0394 bcr1\u0394\/\u0394 strains from 4 other genetic backgrounds. YWP1 has been shown to have antibiofilm activity previously, but CWH8, DAG7, and PGA6 are newly described antibiofilm genes. Our study illustrates the value of strain variation considerations for gene function analysis and the importance of repression targets of biofilm regulators. In addition, our results expand the number of antibiofilm genes.<\/jats:p>","DOI":"10.1093\/genetics\/iyag129","type":"journal-article","created":{"date-parts":[[2026,5,22]],"date-time":"2026-05-22T00:01:58Z","timestamp":1779408118000},"source":"Crossref","is-referenced-by-count":1,"title":["Shared antibiofilm targets of biofilm regulators Wor3 and Bcr1 in\n                    <i>Candida albicans<\/i>"],"prefix":"10.1093","volume":"233","author":[{"given":"Katharina","family":"Goerlich","sequence":"first","affiliation":[{"name":"Department of Microbiology, University of Georgia , Athens, GA 30602 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norma V","family":"Solis","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center , Torrance, CA 90502 ,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott 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