Diplodia ear rot (DER) of maize (Zea mays L.) caused by the fungus, Stenocarpella maydis (Berk.) Sutton has increased in incidence in localized fields over the past decade. My research focused on screening for resistance by examining the development of DER following inoculations prior to flowering, analyzing a diallel cross for DER resistance, and examining the genetic variability of the fungus from isolates collected from the U.S. and the Republic of South Africa. DER developed in maize following inoculations with a spore suspension prior to flowering in both greenhouse and field evaluations. A spore suspension gave a better differentiation of resistance responses than dried preparations of colonized millet, colonized ground popcorn, or kernels from a diseased maize ear, all applied in the whorl 10 to 15 days prior to flowering (V12 for inbreds), and natural occurrence of disease. General combining ability was significant for both 1994 and 1995 growing seasons in an analysis of the F₁ of the diallel cross, indicating that additive gene action may be responsible for resistance and could be introduced into commercial cultivars. Specific combining ability was significant in 1995 and indicates that dominant gene action or epistasis may play role in DER resistance. There were minimal numbers of isozyme polymorphisms found in my S. maydis collection. Two isolates were polymorphic for esterase, two isolates were polymorphic for hexokinase and malate dehydrogenase and one isolate was polymorphic for hexose kinase. Fungi that have limited isozyme polymorphisms often are biotrophs or fungi with formae speciales which are usually limited to one host. These groups of fungi usually have races and this may indicate that a gene-for-gene interaction exists. These findings suggest that i) the whorl inoculation separates genotypes into resistant, intermediate, and susceptible groupings; ii) additive gene action is predominant form of inheritance, and iii) there are few isozyme polymorphisms in the population of S. maydis sampled.