Shared anti-biofilm targets of biofilm regulators Wor3 and Bcr1 in Candida albicans

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ID: 314281
2026
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Abstract
Abstract 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 wor3Δ/Δ bcr1Δ/Δ 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 wor3Δ/Δ, bcr1Δ/Δ, and wor3Δ/Δ bcr1Δ/Δ strains: CWH8, DAG7, JEN2, PGA6, and YWP1. Deletion mutations of CWH8, DAG7, PGA6, or YWP1 enable biofilm formation in vitro in an SC5314-derived wor3Δ/Δ bcr1Δ/Δ strain, and deletion of YWP1 enables biofilm formation in vitro in wor3Δ/Δ bcr1Δ/Δ strains from 4 other genetic backgrounds. YWP1 has been shown to have anti-biofilm activity previously, but CWH8, DAG7, and PGA6 are newly described anti-biofilm 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 anti-biofilm genes.
Reference Key
openalex_W7161948036 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Katharina Goerlich, Norma V Solis, Scott G Filler, Aaron P. Mitchell
Journal current genetics
Year 2026
DOI
10.1093/genetics/iyag129
URL
https://doi.org/10.1093/genetics/iyag129
Keywords Keywords not found

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