The fungus Ustilago maydis causes smut disease in maize. A hallmark of this disease is the formation of large tu-mors which develop on all aerial parts of the plant, leading to stunted growth and significant reductions in crop yield. U. maydis is a biotrophic pathogen that depends on living plant cells to complete its life cycle. U. maydis is related to smut fungi like Ustilago hordei, Ustilago scitaminea and Sporisorium reilianum that are important cereal pathogens and where symptoms develop only in the inflorescence. In all smut fungi pathogenic development is initiated by the filamentous dikaryon that forms infection structures (appressoria) which allow direct penetration of the cuticle, presumably aided by lytic enzymes. During penetration the plasma membrane of the host invaginates and surrounds the infection hyphae, shielding the fungus from direct contact with the host cytoplasm. Although hyphae traverse plant cells, there are only limited host defense responses and the infected plant tissue remains alive until late in the infection process when fungal proliferation occurs mostly in the apoplast. Initial plant defense responses, presumably triggered by fungal PAMPs, must actively be suppressed by the pathogen during colonization. This is accomplished by secreted effector molecules that either have a function in the tight interaction zone between fungal hyphae and host plasma membrane or are translocated to host cells. Our work during the period of the report has focused on the early phase of fungal development, i. e. fungal differentiation after contact with the leaf surface, the downstream signaling cascades and on how secreted effectors shape the biotrophic interaction.