The diffusional barrier formed between phagocyte integrin and fungal glucans preserves the microbiostatic phagocytic environment generated during the frustrated phagocytosis of Candida albicans hypha.

Candida albicans cells respond in two distinct ways to fluconazole exposure where cells enter the Ribo-dominant state characterized by an upregulation of ribosomal-related proteins and processes, or cells enter the Stress-dominant state characterized by the upregulation of stress responses.

Rewiring of transcriptional circuits can preserve a basic output yet alter almost all of the circuit's quantitative and qualitative features.

Loss-of-heterozygosity mutations, but not aneuploidies, are linked to the evolution of drug resistance in Candida albicans isolated from immunocompromised patients.

Previously uncharacterized long repeat sequences are associated with significant genome variation that can increase fitness and promote antifungal drug resistance in diverse isolates of Candida albicans.

Novel segmental chromosome amplifications in Candida albicans provide rapid adaptation to the most widely used antifungal drugs.

Rapid evolutionary rewiring of the meiosis transcription network facilitated a switch in the function of a master regulator from regulating meiosis to regulating biofilm formation.

NETs induction, a central component of the innate immune response, utilises assorted signalling pathways as demonstrated through the analysis of healthy and patient neutrophils treated with five distinct stimuli.

The molecular mechanism that candidalysin uses to perforate membranes is unraveled, which opens the door to the rational design of inhibitors against candidiasis.

An intravital screen identifies the transcription factors that govern gene expression of the human fungal pathogen Candida albicans during filamentation in a mammalian host.