|Abstract:||Although sweet corn (Zea mays L.) with the shrunken-2 (sh2) endosperm mutation has broad consumer appeal due to its sweet taste and long refrigerator life, its cultivation has been plagued by emergence and seedling vigor problems. The high sucrose content of sh2 kernels, accumulated at the expense of starch reserves, is one of several factors associated with the poor vigor of sh2 hybrids. Another factor affecting vigor is infection of sh2 kernels by fungal pathogens, especially Fusarium moniliforme Sheldon (teleomorph: Gibberella fujikuroi (Sawada) Wollenw.). The objectives of this research were to determine the effects of kernel carbohydrate content and post-pollination silk condition on kernel infection by F. moniliforme, to determine the effects of kernel carbohydrate content and infection by F. moniliforme on seedling emergence, to identify sources of resistance to kernel infection by F. moniliforme, and to determine the site of resistance. It was found that kernel carbohydrate content did not significantly affect kernel infection by F. moniliforme. The length and color of exposed silks at the time of inoculation were associated with the incidence of kernel infection. Inbreds with green, actively growing silks at the time of inoculation had less kernel infection than those with short, senescent silks. Kernel infection by F. moniliforme was the most important variable affecting sweet corn inbred emergence, although symptomatic and asymptomatic infection of kernels accounted for just 39 and 30% of the variation in emergence, respectively. Kernel carbohydrate fractions did not have individual effects on inbred emergence. However, many of the carbohydrate variables did significantly affect emergence when the variance in emergence due to kernel infection by F. moniliforme was accounted for in multiple regression models. Several sources of partial resistance to kernel infection by F. moniliforme were identified among sweet corn inbreds that exhibited good emergence. In crosses of resistant x susceptible inbreds, a strong maternal influence on resistance to kernel infection by F. moniliforme was observed. The observed response was attributed to factors operative in the maternal tissues, e.g., the silk, pericarp, or placento-chalazal region. The genotype of the cytoplasm, endosperm or embryo did not affect kernel infection by F. moniliforme.