Submitted to: Canadian Journal of Plant Science
Publication Type: Peer reviewed journal
Publication Acceptance Date: 12/28/1998
Publication Date: N/A
Citation: Interpretive Summary: Red clover is a perennial legume used throughout the northcentral and northeast regions of the U.S. as forage for animal agriculture. However, its' longevity in hay and pasture fields is reduced by a fungus effecting the roots and crowns of the plants. The disease is called Fusarium Wilt and is caused by the organism Fusarium oxysporum. We have determined that genetic resistance in red clover to the organism is controlled by many genes. By using appropriate selection and crossing procedures for the resistance genes in red clover, we have been able to increase resistance to the organism by 30%. This new red clover germplasm with greater resistance to the organism will be made available to the plant breeding industry to develop varieties of red clover with greater longevity and productivity.
Technical Abstract: In Wisconsin, Fusarium oxysporum, Schlect., a pathogen causing vascular wilt, is the most prevalent fungal pathogen recovered from diseased red clover (Trifolium pretense L.) plants. This study was conducted to determine the mode of inheritance for red clover resistance to this pathogen and to develop resistant germplasm. Virulent isolates of this pathogen, collected from red clover plants at the Ashland Research Station Ashland, Wisconsin, were used to screen three populations, the red clover cultivars Arlington and Marathon, and the C11 germplasm, for resistant plants. Plants were inoculated with the pathogen and evaluated for reaction using a Disease Severity Index (DSI) score from 1 to 5 (1 = no reaction, 5 = plant dead). Selected plants from each cycle were intercrossed to produce subsequent generations. After two and three cycles of selection the developed populations were simultaneously evaluated for gain from selection. The gain from selection for resistance in these populations (cycle 0 minus cycle 2) ranged from 0.31 - 0.48, 0.12 - 0.75, and 0.13 - 0.83 DSI units, respectively, for Arlington, Marathon, and C11. Estimated narrow sense heritabilities based on Cycle 1 and Cycle 2 progeny were, respectively, 0.20 and 0.37 for Arlington, 0.15 and 0.13 for Marathon, and 0.06 and 0.17 for C11. These results indicate that resistance is a quantitative trait controlled by many loci, each contributing some portion to overall resistance in the host.