RESUMO
Sclerotinia blight, caused by the soilborne fungus Sclerotinia minor Jagger, is a major disease of peanut (Arachis hypogaea L.) in parts of west Texas. Previous reports have indicated that annual weed species may serve as collateral hosts for S. minor (2). Several Ipomoea spp. are commonly found in peanut fields throughout the region. In September of 2007, Ipomoea hederacea and I. coccinea plants with bleached, shredded stems, and signs of black sclerotia were collected from a field known to be infested with S. minor. Symptomatic stem sections were rinsed in tap water, surface disinfested in 0.5% sodium hypochlorite for 1 min, air dried, and plated on potato dextrose agar (PDA). Pure cultures of S. minor consisting of white, fluffy mycelia and small (<2 mm), black, irregular sclerotia were consistently recovered. Pathogenicity tests were conducted by wound-inoculating healthy I. hederacea and I. coccinea transplants (n = 3) with agar plugs obtained from the edges of actively growing S. minor cultures. Plants were incubated in a dew chamber at 20°C and 95% relative humidity for 5 days. Plants inoculated with sterile PDA plugs served as controls (n = 3). A similar test was conducted using the susceptible peanut cultivar Flavorunner 458. Characteristic symptoms of Sclerotinia blight (3) were observed on all inoculated weed and peanut plants; whereas, the controls remained healthy. Pathogenicity tests were repeated with similar results. Cultures of S. minor were obtained from all symptomatic tissues, fulfilling Koch's postulates. These results indicate that I. hederacea and I. coccinea are additional hosts of S. minor and that sclerotia produced on infected plants can significantly augment soil inoculum. S. minor has been observed to infect I. batatas seedlings in New Jersey (1); however, this to our knowledge is the first report of S. minor infecting Ipomoea spp. in Texas. Therefore, weed management should inevitability be a part of disease management strategies for the control of Sclerotinia blight in peanut. References: (1) Anonymous. Index of Plant Diseases in the United States. USDA Handb. No. 165, 1960. (2) J. E. Hollowell et al. Plant Dis. 87:197, 2003. (3) D. M. Porter and H. A. Melouk. Sclerotinia blight. Page 34 in: Compendium of Peanut Diseases. 2nd ed. N. Kokalis-Burelle et al., eds. The American Phytopathologicial Society, St. Paul, MN, 1997.
RESUMO
Herbicidal activity of aryloxyphenoxypropionate and cyclohexanedione herbicides (graminicides) has been proposed to involve two mechanisms: inhibition of acetyl-coenzyme A carboxylase (ACCase) and depolarization of cell membrane potential. We examined the effect of aryloxyphenoxypropionates (diclofop and haloxyfop) and cyclohexanediones (sethoxydim and clethodim) on root cortical cell membrane potential of graminicide-susceptible and -tolerant corn (Zea mays L.) lines. The graminicide-tolerant corn line contained a herbicide-insensitive form of ACCase. The effect of the herbicides on membrane potential was similar in both corn lines. At a concentration of 50 [mu]M, the cyclohexanediones had little or no effect on the membrane potential of root cells. At pH 6, 50 [mu]M diclofop, but not haloxyfop, depolarized membrane potential, whereas both herbicides (50 [mu]M) dramatically depolarized membrane potential at pH 5. Repolarization of membrane potential after removal of haloxyfop and diclofop from the treatment solution was incomplete at pH 5. However, at pH 6 nearly complete repolarization of membrane potential occurred after removal of diclofop. In graminicide-susceptible corn, root growth was significantly inhibited by a 24-h exposure to 1 [mu]M haloxyfop or sethoxydim, but cell membrane potential was unaffected. In gramincide-tolerant corn, sethoxydim treatment (1 [mu]M, 48 h) had no effect on root growth, whereas haloxyfop (1 [mu]M, 48 h) inhibited root growth by 78%. However, membrane potential was the same in roots treated with 1 [mu]M haloxyfop or sethoxydim. The results of this study indicate that graminicide tolerance in the corn line used in this investigation is not related to an altered response at the cell membrane level as has been demonstrated with other resistant species.
