Hidden allies: how extracellular vesicles drive biofilm formation, stress adaptation, and host-immune interactions in human fungal pathogens.

Pathogenic fungi pose a significant threat to human health, especially given the rising incidence of invasive fungal infections and the emergence of drug-resistant strains. This requires the development of vaccines and the advancement of antifungal strategies. Recent studies have focused on the roles of fungal extracellular vesicles (EVs) in intercellular communication and host-pathogen interactions.

Negative regulation of biofilm development by the CUG-Ser1 clade-specific histone H3 variant is dependent on the canonical histone chaperone CAF-1 complex in Candida albicans.

The CUG-Ser1 clade-specific histone H3 variant (H3V ) has been reported to be a negative regulator of planktonic to biofilm growth transition in Candida albicans. The preferential binding of H3V at the biofilm gene promoters makes chromatin repressive for the biofilm mode of growth. The two evolutionarily conserved chaperone complexes involved in incorporating histone H3 are CAF-1 and HIRA.

The Candida albicans biofilm gene circuit modulated at the chromatin level by a recent molecular histone innovation.

Histone H3 and its variants regulate gene expression but the latter are absent in most ascomycetous fungi. Here, we report the identification of a variant histone H3, which we have designated H3VCTG because of its exclusive presence in the CTG clade of ascomycetes, including Candida albicans, a human pathogen. C.

A surprising role for the Sch9 protein kinase in chromosome segregation in Candida albicans.

The AGC kinase Sch9 regulates filamentation in Candida albicans. Here, we show that Sch9 binding is most enriched at the centromeres in C. albicans, but not in Saccharomyces cerevisiae.