Anna M. Selmecki

This study uses CRISPR-activation to identify genes with fitness effects in Candida albicans isolates, revealing resistance genes and vulnerabilities associated with copy number variants.

This study shows that micafungin exposure selects for multidrug resistance in C. lusitaniae through mutations in ERG3, leading to sterol reprogramming and cell wall remodeling.

This study analyzes genomic variation in serial Candida albicans isolates from patients, identifying aneuploidy, polyploidy, and loss of heterozygosity as factors driving antifungal drug tolerance.

This study analyzes Candida bloodstream isolates from multiple hospitals, identifying species distribution, antifungal resistance patterns, and within-patient variability in drug susceptibility.

This study shows how azole resistance in Candida albicans evolves through copy number variation followed by KSR1 loss of heterozygosity, resulting in a >500-fold resistance increase.

This study identifies ERG251 mutations that confer azole tolerance and pleiotropic effects on stress responses and filamentation in C. albicans.

This study evaluates the fitness costs and benefits of trisomy in Candida albicans across various stress conditions, finding that specific aneuploids confer growth advantages under host-relevant stresses.

The paper shows that trisomy of chromosomes 5 or 6 in Candida albicans during oropharyngeal infection leads to a commensal-like phenotype with reduced virulence.