The AP-1 adaptor complex is required for cell surface modifications and the survival of Cryptococcus neoformans in phagocytic cells.

The pathogenic yeast Cryptococcus neoformans causes life-threatening meningoencephalitis in individuals with compromised immune systems. The ability of the fungus to cause disease depends on key cell-surface features, such as a polysaccharide capsule that protects it from the mammalian immune system. However, the mechanisms by which C. neoformans traffics polysaccharide capsule, melanin, and other materials to the cell surface are poorly understood. In this study, we employed mutants lacking specific subunits of the adaptor protein complex 1 (AP-1) to investigate its role in the elaboration of virulence-related materials at the cell surface. Importantly, the mutants displayed multiple defects, including alterations in capsule size and cell morphology, and defects in melanin production and urease secretion. Together, these results support the key observation that the AP-1 complex is required for C. neoformans survival in phagocytic cells. Together, our findings provide insights into the endomembrane trafficking machinery required for fungal pathogenesis.