Scott G. Filler

This study shows that fungal-induced immunosurveillance remodels the oral mucosal barrier via a non-canonical IL-22 receptor complex, enhancing resistance to Candida albicans colonization.

This study shows that HosA, a histone deacetylase in A. fumigatus, regulates stress resistance, host cell interactions, and virulence by modulating gene expression related to secondary metabolism and energy metabolism.

This study identifies a metabolic-epigenetic mechanism in oral epithelial cells that enhances protection against fungal infection through proline catabolism and mitochondrial function.

This study shows that Chr7 trisomy in Candida albicans affects colonization and virulence differently depending on strain background and homolog identity.

This paper shows EGFR signaling is essential for host defense against invasive aspergillosis, as its inhibition worsens infection outcomes in immunosuppressed mice.

This study identifies sulfated glycosaminoglycans as targets of candidalysin, a virulence factor in C. albicans, and shows that blocking these interactions can protect epithelial cells from fungal damage.

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 impact of read length and pairing on differential expression analysis in host-pathogen interactions, finding 54-bp paired reads most robust and 36-bp single reads suitable for bacterial samples.

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.

This study compares enrichment techniques for multi-species RNA-Seq, finding that targeted enrichment with Agilent SureSelect improves read mapping to target organisms.

This study shows that Candida albicans rapidly generates genotypic and phenotypic diversity in the mouse oral cavity, with higher mutation rates compared to in vitro conditions.