Fusarium graminearum is the causal agent of ear blight disease of cereals. Infection occurs at anthesis when ascospores and/or conidia directly penetrate exposed anther and ovary tissue. The hemibiotrophic hyphae colonize floral tissues and developing grains to cause premature ear senescence. During infection, Fusarium hyphae can also produce hazardous trichothecene mycotoxins, thereby posing a threat to human and animal health and safety. The Fusarium MAP1 gene was identified using a PCR approach by its homology to a known pathogenicity gene of Magnaporthe grisea, the mitogen-activated protein kinase gene PMK1. Gene replacement F. graminearum map1 mutants were non-pathogenic on wheat flowers and roots, and also could not infect wounded wheat floral tissue or tomato fruits. Unlike the wild-type strain, map1 mutant inoculations did not compromise grain yield. Map1 mutants lost their ability to form perithecia in vitro, but their rate of asexual conidiation was unaffected. DON mycotoxin production in planta was still detected. Collectively, the observed phenotypes suggest that the Map1 signalling protein controls multiple events in disease establishment and propagation. Novel approaches to control Fusarium ear blight disease by blocking perithecial development are discussed.