Submitted to: Trifolium Conference Abstract & Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 6/4/1998
Publication Date: N/A
Interpretive Summary: White clover is a widely grown forage legume in pastures of the southeastern USA. However, a major problem that limits its use is that stands often do not persist for more than 2-3 years after seeding. White clover then rapidly disappears from pastures, and it must be reseeded at significant cost to the farmer if its presence is to be maintained. Viruses and fungal diseases that weaken or kill infected plants are known to be major individual causes for limited persistence of white clover. However, it is not known whether viruses and fungal diseases interact to cause more rapid death of plants when both are present together. In this study, the effects of infection by a common virus of white clover, peanut stunt virus (PSV), on development of disease by two fungal pathogens, were evaluated in excised leaf tissues. Individual white clover plants were cloned (increased and replicated by rooting stem cuttings), and half of the clones were infected with PSV. Samples of leaf tissue from plants with and without PSV were inoculated with each of the fungal pathogens, observed daily, and scored according to the rate at which fungal disease symptoms appeared. In two experiments with one fungal pathogen and four with the second, differences in disease development between leaves of white clover plants with and without PSV were observed in only one experiment, where greater fungal disease occurred in leaves from plants infected with PSV. These results indicate that in leaf tissue of white clover, infection by PSV usually does not cause greater disease development by the two fungal pathogens. Results further suggest that PSV and the two fungal pathogens usually act idependently to limit persistence of white clover in pastures of the southeastern USA.
Technical Abstract: Peanut stunt virus (PSV) and two fungal pathogens, Macrophomina phaseolina and Sclerotium rolfsii, are considered to be major individual limiting factors for persistence of white clover in pastures of the southeastern USA. Although PSV and the fungal pathogens frequently occur together on white clover, their potential interactions in symptom development have not been evaluated. This study was undertaken to determine whether systemic infection of white clover by PSV predisposes leaf tissue to more rapid and extensive parasitism by M. phaseolina and S. rolfsii. Thirty-three geno- types of white clover were cloned by rooting vegetative cuttings. Half of the clones of each genotype were mechanically inoculated with PSV, and the presence and absence of systemic infection in all plants was confirmed by enzyme-linked immunosorbent assay. Discs (12 mm dia) of leaf tissue from each genotype (+) and (-) PSV were placed individually in petri dishes (3.5 cm diameter) and inoculated in separate experiments with infested agar discs from colonies of M. phaseolina and S. rolfsii. Leaf discs were maintained under growth lights, observed daily for 1 week, and scored according to the rate and extent of fungal symptom development. In each of two experiments with M. phaseolina, significant (P=0.05) differences in symptom development were observed between white clover genotypes but not between genotypes (+) or (-) PSV. In four experiments with S. rolfsii, significant differences between genotypes were observed in each experiment, but a significant difference between genotypes (+) and (-) PSV was observed in only one experiment. These results indicate that systemic infection of white clover by PSV usually does not predispose leaf tissue to more severe symptom development by M. phaseolina or S. rolfsii.