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Etiology

Infection of Two Endosperm Mutants of Sweet Corn by Fusarium moniliforme and its Effect on Seedling Vigor. Roger C. Styer, Vegetable Crops Department, Institute of Food and Agricultural Science, University of Florida, Gainesville 32611; Daniel J. Cantliffe, Vegetable Crops Department, Institute of Food and Agricultural Science, University of Florida, Gainesville 32611. Phytopathology 74:189-194. Accepted for publication 11 August 1983. Copyright 1984 The American Phytopathological Society. DOI: 10.1094/Phyto-74-189.

Kernels of hybrid sweet corn plants with the recessive shrunken-2 (sh2) gene became heavily infected with Fusarium moniliforme in the field earlier than kernels of hybrid plants with the standard sugary (su) gene. Mature ears of both mutants inoculated 10 days postpollination (DPP) with F. moniliforme had higher levels of rot and seed infection than those inoculated later in development. In sh2 seeds, the pathogen appeared to enter through small cracks in the pericarp or by appressoria. The fungus spread throughout pocketlike areas between the pericarp and aleurone layer, and eventually moved into the endosperm and embryo. Infection increased the number of abnormal su seedlings and reduced seedling growth of sh2 seeds germinated under optimum conditions. Germination of infected sh2 seeds was lower in a cold soil test and growth rates were reduced compared to those observed under optimum conditions. Poor seed and seedling vigor of sh2 was due, in part, to infection with F. moniliforme, but this infection did not appear to be the primary factor involved in the reduction in vigor. Under stress conditions, uninfected sh2 seeds had less germination and vigor than uninfected su seeds.