The pathogenic life cycle of the rice blast fungus involves a series of morphogenetic changes, essential for its ability to cause disease. The mutation was identified > 25 years ago, and affects the shape and development of diverse cell types in , including conidia, appressoria, and asci. All attempts to clone the gene by map-based cloning or complementation have failed over many years. Here, we report the identification of by a combination of bulk segregant analysis and comparative genome analysis. encodes a GTPase-activating protein, which regulates Ras signaling during infection-related development. Targeted deletion of results in abnormal, nonadherent conidia, impaired in their production of spore tip mucilage. Smo1 mutants also develop smaller appressoria, with a severely reduced capacity to infect rice plants. is necessary for the organization of microtubules and for septin-dependent remodeling of the F-actin cytoskeleton at the appressorium pore. Smo1 physically interacts with components of the Ras2 signaling complex, and a range of other signaling and cytoskeletal components, including the four core septins. is therefore necessary for the regulation of RAS activation required for conidial morphogenesis and septin-mediated plant infection.