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The Disease Cycle and Fungus-Host Relationships in Dallisgrass Ergot. E. S. Luttrell, Department of Plant Pathology, University of Georgia, Athens, GA 30602; Phytopathology 67:1461-1468. Accepted for publication 20 June 1977. Copyright 1977 The American Phytopathological Society, 3340 Pilot Knob Road, St. Paul, MN 55121. All rights reserved.. DOI: 10.1094/Phyto-67-1461.

Germ tubes from conidia of Claviceps paspali penetrate between cells of stigmas or styles of Paspalum dilatatum within 4 hr and invade the ovary through the style. In 2-3 days, intercellular hyphae permeate the ovary and break out between the epidermal cells. At 4 days, a thick plectenchymatous stroma envelops the disintegrating ovary. Conidia produced on the surface of the stroma ooze from infected florets in drops of honeydew by the 5th or 6th day. The extramatrical stroma develops into the mature, globose, white-to-brown ergot sclerotium in 2-3 wk. The ovary serves primarily as a portal of entry for the pathogen and is destroyed soon after infection. The fungus establishes a continuing compatible relationship with living host cells in a narrow interface between fungus stroma and noninvaded host tissue in the receptacle of the floret. Primary disease cycles are initiated by airborne ascospores forcibly discharged from perithecia produced on clavae arising from overwintered sclerotia. At least 6 wk of exposure to 5 C is required to break dormancy of sclerotia. Inoculations with conidia are most effective at anthesis. A 2-hr dew period is sufficient for infection after floret closure.

Additional keywords: pathological histology, Ascomycetes, Clavicipitaceae.