Biofilms are microbial communities constituting a class of soft biomatter with characteristic viscoelasticity. Biofilm viscoelastic properties can be measured through rheology, which quantifies the deformation of objects in response to external forces, such as flow and shear stress. Biofilm rheological properties can significantly impact the outcomes of microbial infection, and the rheological response of bacterial biofilms has been studied with interest. The rheological phenotypes of fungal biofilms, however, have been neither quantified extensively nor genetically dissected. We have developed methods to quantify the rheology of colony biofilms generated by the primary opportunistic human fungal pathogen Candida albicans . Here, we aim to identify genes that underlie rheological phenotypes in C. albicans by analyzing a panel of deletion mutants impaired in cell wall structure or extracellular matrix (ECM) production. We find that increased elastic moduli, indicative of higher viscoelasticity, are evident in strains singly deleted for the ALG11 , KRE5 , and PMR1 genes, with complementation strains showing wild-type phenotypes. ALG11 encodes α-1,2-mannosyltransferase, and KRE5 encodes a UDP-glucose:glycoprotein glucosyltransferase. PMR1 encodes a secretory pathway calcium pump. The respective deletion mutants exhibit a smooth biofilm morphology on agar, with reduced hyphae, decreased ECM, and decreased fluconazole resistance. Transcriptional profiling of these strains identifies altered expression of genes affecting cell membrane/cell wall biology, lipid metabolism, and filamentous development. Collectively, the data present C. albicans biofilm rheology as a distinct phenotype affected by ECM production, filamentous development, and cell wall architecture, while identifying genes for the further mechanistic investigation of fungal biofilm viscoelasticity.
Abriat et al. (Fri,) studied this question.