Submitted to: American Peanut Research and Education Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: May 15, 2004
Publication Date: December 1, 2004
Citation: Saude, C.N., Melouk, H.A., Chenault, K.D., Meador, C.B. 2004. Oxalic acid production by isolates of Sclerotium rolfsii and their pathogenicity on peanut [abstract]. In: Proceedings of the American Peanut Research and Education Society, July 13-16, 2004, San Antonio, Texas. 36:51. Technical Abstract: Seventeen isolates of Sclerotium rolfsii from various vegetables, peanut and wheat were evaluated for their pathogenicity on Okrun, an S. rolfsii-susceptible peanut cultivar, and for oxalic acid (OA) production in liquid culture. Okrun peanut was grown in the greenhouse for six weeks at which time organic debris was removed from the soil surface and plants were watered to saturation. A 1-cm disc of filter paper was placed around the base of each stem and three sclerotia were placed on the filter paper adjacent to and touching the stem. Plants were placed in chambers maintained at 28-30 C° and 100% relative humidity for fourteen days. Sclerotial germination was recorded four days after inoculation and disease severity was assessed at two-day intervals thereafter. A pathogenicity scale of 1-6 was used with 1 being no mycelia on stem and 6 being a dead plant. Oxalic acid production by isolates was measured by growing S. rolfsii in liquid culture. Flasks containing 100 ml of potato dextrose broth (PDB) were inoculated with three 0.5-cm mycelial plugs from three-day old cultures of S. rolfsii and were placed on a rotary shaker for six days. Mycelial mats were removed on day 2 through day 6 and OA concentration was determined in culture filtrates using a diagnostic analysis kit (Sigma). All isolates, except wheat isolate from Oklahoma, were pathogenic to peanut. All isolates produced significant amounts of OA on PDB. Mycelial biomass of isolates was highly correlated to the amounts of OA produced in liquid culture. Our data on pathogenicity of S. rolfsii and OA production suggest that OA is not he sole factor determining pathogenicity.