FIG 2 .

Role of glycosphingolipids in Aspergillus biology and pathogenesis. The filamentous fungus Aspergillus is ubiquitously dispersed in the environment, and the asexual sporulation produces airborne conidia. The inhalation of Aspergillus conidia (1) by a severely immunocompromised host leads to germination and extensive hyphal growth in the lungs (2), which can culminate in disseminated infection through the bloodstream. In growing conidia (1), PhCer and Δ8-9-Me-Cer are produced in the endoplasmic reticulum (ER) and transported to the Golgi apparatus for synthesis of GSLs, such as GalCer, GlcCer, and IPC. The inhibition of steps of this pathway, by gene deletion or antifungal drugs, prevents germination or leads to loss of viability. In the absence of inhibition, IPC, GlcCer, and GalCer can be directed to the active sites of the plasma membrane, playing a role in polarized growth and contributing to fungal invasion (2). The asterisk indicates that after synthesis, IPC can achieve further complexity through the addition of glucosamine, mannose, and galactofuranose residues before being anchored in the plasma membrane.