A metabolic checkpoint controls hyphal development in Candida albicans via nitric oxide signaling

We investigated the roles of mitochondrial dynamics in hyphal growth of C. albicans using the small molecule inhibitor MDIVI-1. Strikingly, the small molecule inhibitor represses both the yeast-to hyphae transition and ongoing filamentation, and its effects on morphogenesis can be uncoupled from general growth inhibition. RNAseq experiments of inhibitor-treated cells coupled with Candida mutant analyses suggest the existence of a novel mechanism of action to represses hyphal growth. The inhibitor was protective to host cells, increasing the survival of bone-marrow derived macrophages in ex vivo macrophage-Candida infection assays, suggesting it has potential as a therapeutic. Overall design: Analysis of RNA-seq in C. albicans