Frogeye leaf spot of soybean (FLS) (Glycine max (L.) Merr.), caused by Cercospora sojina Hara, was first detected in Virginia in 1942 (1). During the 2008 growing season, a FLS survey was conducted in soybean fields in Virginia. This was the first FLS race survey conducted in Virginia. Typical frogeye leaf spot symptoms, as reported by Phillips (4), were observed on soybean leaves in Westmoreland County. During 2008, Westmoreland County planted 7,365 ha of soybean. Symptomatic leaves were collected from V06-1891, V06-1365, V05-4394, V04-8405, and Hutcheson cultivars from plants in growth stages R5 to R6. Leaves were placed in a moist chamber for 24 h at 21°C with 12-h light to induce sporulation. C. sojina was only recovered from V06-1365. Conidia were removed from the leaves, placed into V8 juice agar amended with rifampicin (10 mg ml–1) and ampicillin (0.25 g liter–1) and incubated at 21°C with 12-h light. Cultures with dark pigmentation and presence of conidia were observed after 3 weeks. Conidia matched the description of C. sojina (4). Conidia had three to nine septa, were hyaline, elongate to fusiform, and measured 3 to 6 × 25 to 40 μm. Race identification was conducted using the set of differentials reported by Mian et al. (3). Spores for inoculation were produced on soybean stem lima bean agar (SSLBA) media. Ten-centimeter-diameter pots, each containing four plants, were used. The test was conducted twice in a complete randomized design with three replications. Seedlings were inoculated at the V3 growth stage with a spore suspension of 6 × 104 spores/ml. Control plants were sprayed with sterile distilled water. Plants were placed in a greenhouse bench humidity chamber at 21°C for 72 h. Disease rating was conducted 14 days after inoculation. Since the resistance to FLS is known to be controlled by single dominant genes, the FLS was scored as a qualitative trait (i.e., resistant versus susceptible) as previously done by Mian et al. (2). Plants that showed numerous, large, spreading lesions were classified as susceptible and each plant was given a score of 1. Plants that showed no lesions or only small lesions or flecks were classified as resistant and each plant was given a score of 0. Control plants remained healthy. On the basis of the reaction response of the isolate on the set of differentials and comparison with the proposed race designations of Mian et al. (3), the isolate was classified as race 11. Race 11 shows compatible reaction (susceptibility) on the soybean cv. Lincoln, which is the source of Rcs1 resistance gene, and incompatible reactions (resistance) on cvs. Peking, Davis, and Kent. The latter two cultivars are sources of the Rcs3 and Rcs2 genes, respectively. Successful development of soybean cultivars with FLS resistance not only depends on knowledge of the presence of resistance genes, but also on the understanding of the pathogen population structure. To our knowledge this is the first report of C. sojina race 11 from soybean in Virginia. Resistance to this race is conditioned by Rcs2, Rcs3, and the single dominant gene in Peking (3). We recommend use of Rcs3 and Rcs2 genes and the single dominant gene in Peking for resistance to FLS in Virginia.
References: (1) S. B. Fenn. Plant Dis. Rep. 26:383, 1942. (2) M. A. R. Mian et al. Crop Sci. 39:1687, 1999. (3) M. A. R. Mian et al. Crop Sci. 48:14, 2008. (4) D. V. Phillips. Page 20 in: Compendium of Soybean Diseases. 4th ed. The American Phytopathological Society. St. Paul, MN, 1999.