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Resistance

Distribution and Growth of Fusarium oxysporum f. sp. lycopersici Race 1 or Race 2 within Tomato Plants Resistant or Susceptible to Wilt. W. S. Conway, Research Assistant, Department of Botany and Plant Pathology, University of New Hampshire, Durham, NH 03824, Present address of senior author: Biology Department, Delhi University, Delhi, NY 13753; W. E. MacHardy, Associate Professor, Department of Botany and Plant Pathology, University of New Hampshire, Durham, NH 03824. Phytopathology 68:938-942. Accepted for publication 7 November 1977. Copyright 1978 The American Phytopathological Society, 3340 Pilot Knob Road, St. Paul, MN 55121. All rights reserved.. DOI: 10.1094/Phyto-68-938.

The distribution and growth rate of Fusarium oxysporum f. sp. lycopersici race 1 or race 2 in near-isogenic tomato lines Improved Pearson (IP) and Pearson VF-11 (VF) were investigated. Cultivar IP is susceptible to both races; VF is resistant to race 1 but susceptible to race 2. The three susceptible combinations (IP/race 1; IP/race 2; VF/race 2) exhibited similar patterns of pathogen population increases within the taproot/hypocotyl vascular tissue followed by extensive invasion and build-up within epicotyl vascular bundles. In contrast, continual distribution of race 1 within VF did not occur. The extensive invasion and build-up of race 2 within VF epicotyls, compared to the limited invasion of race 1 in VF, suggests that the virulence of race 2 toward VF is related to its capacity to overcome the resistance mechanism that normally localizes infections within the root/hypocotyl region. Antifungal compounds reported to be present within the upper stem do not appear to be effective in limiting the pathogen and preventing symptom development once the localization process is overcome and there is extensive hypocotyl colonization and subsequent pathogen spread, within many vessels, to the epicotyl. The possible contributions of host-produced fungal inhibitors and physical barriers to fungal growth and movement are discussed.

Additional keywords: resistance mechanism, vascular wilt diseases.