The contribution of transcription factor ROB1 to the pathophysiology of C. albicans-induced candidal infections biorxivpreprint uiowa UWMadison universityofga BrownUniversity infection disease pathogen fungus
By Pooja Toshniwal PahariaJun 20 2023Reviewed by Danielle Ellis, B.Sc. In a recent study posted to the bioRxiv* preprint server, researchers evaluated the function of the zinc finger transcription factor ROB1 and its two phenotypically distinct alleles in the pathogenesis of Candida albicans infections.
Among humans, Candida albicans can cause mucosal candidiasis involving oral and genitourinary mucosae and invasive candidiasis involving the blood, central nervous system , and abdominal organs such as the spleen and liver. The team generated deletion mutants of ROB1 in four clinical isolates of Candida albicans with different filamentation phenotypes, i.e., P76067, P75010, P57055, and P87, to assess their effects on filamentation at 30 °C and 37 °C and investigate whether the impact of ROB1 on filamentation varied with strain background.
Sanger sequencing of ROB1 was performed for the six isolates to determine their genotypes. ROB1 allelic filamentation was also compared in vivo by intravital imaging of ROB1 mutant-infected murine subcutaneous ear tissues. Biofilm formation was assessed in a murine model of C. albicans vascular catheter infections, a disseminated candidiasis model, and an oropharyngeal candidiasis model.
ROB1 affected the formation of biofilms and hyphal morphogenesis based on the inducing conditions and the strain of C. albicans. The rob1∆∆ genetic mutant reduced the reference rob1∆∆ strain filamentation on the Spider culture medium at 37 °C; at 30 °C, the ROB1 mutant showed altered wrinkling patterns in the centre with peripheral invasion, whereas, at 37 °C, smooth colonies were observed lacking peripheral invasion.
The RNA-seq analysis showed the downregulation of 10 ROB1-dependent hypha-specific genes in the rob1∆∆ genetic mutant in the culture mediums, including the hyphal wall protein-1 , hyphal-regulated gene-1 , SAP-6, ECE-1, and WOR-3. On the contrary, none of the genes were upregulated.
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