ABSTRACT
Cephalosporium stripe (CS) (2) was identified in a commercial field of winter wheat (Triticum aestivum) near Riner, Montgomery County, Virginia in May 2006. Nearly 15% of the field was severely affected. Broad, yellow-brown stripes were observed on the leaf blades of affected plants, and many plants were stunted and had ripened prematurely. Symptomatic plants were associated with low acidic (pH 5.2), wet spots of the field. Leaves and nodes of affected plants were surface disinfested for 1 min in 5% sodium hypochlorite, plated on corn meal agar (CMA), and incubated at 20°C for 5 days. Cephalosporium gramineum was isolated from numerous plants. Cultures of the fungus produced hyaline conidiophores approximately 5 µm long and unicellular conidia 3 to 7 µm long. Aqueous suspensions of mycelia and conidia were prepared from pure cultures. Several spring wheat cultivars were wounded by severing the root mass and were inoculated when the fifth stem node was detectable (35 on Zadoks scale). Noninoculated plants were wounded as controls. Plants were kept in the greenhouse at temperatures of 22 to 27°C. After 14 days, inoculated plants produced symptoms of CS, and the fungus was reisolated from the leaves of these plants. No symptoms were observed on noninoculated control plants. Though CS had been observed in Virginia in research nurseries (1), to our knowledge, this is the first confirmed report of the disease in a commercial wheat field in Virginia. References: (1) J. B. Jones et al. Plant Dis. 64:325, 1980. (2) C. M. Stiles and T. D. Murray. Phytopathology 86:177, 1996.
ABSTRACT
Breeding maize for gray leaf spot (GLS) resistance has been hindered by the quantitative nature of the inheritance of GLS resistance and by the limitations of selection under less than optimumal disease pressure. In order to identify the quantitative trait loci (QTLs) controlling GLS resistance, a cross was made between B73 (susceptible) and Va14 (resistant) to generate a large F2 population. Six GLS disease assessments were made throughout the disease season for over 1000 F2 plants in 1989, and for 600 F2-derived F3 lines replicated in two blocks in 1990. RFLP analysis for78 marker loci representing all ten maize chromosomes was conducted in 239 F2 individuals including those with the extreme GLS disease phenotypes. The GLS disease scores of the three field evaluations, each averaged over six ratings, were separately used for the interval mapping in order to determine the consistency of the QTL effects. The heavy GLS disease pressure, meticulous disease ratings, and large population size of this study afforded us the sensitivity for detecting QTL effects. QTLs located on three chromosomes (1, 4, and 8) had large effects on GLS resistance, each explaining 35.0-56.0%, 8.8-14.3%, and 7.7-11.0% of the variance, respectively. These three QTL effects were remarkably consistent across three disease evaluations over 2 years and two generations. Smaller QTL effects were also found on chromosomes 2 and 5, but the chromosome-5 effect might be a false positive because it was not repeatable even in the same location. The chromosome-1 QTLs had the largest effect or highest R(2) reported for any quantitative trait to-date. Except for the chromosome-4 gene, which was from the susceptible parent B73, the resistance alleles at all QTL were derived from Va14. The resistance QTLs on chromosomes 1 and 2 appear to have additive effects, but those on chromosomes 4 and 8 are dominant and recessive, respectively. Significant interaction between the QTLs on chromosomes 1 and 4 was detected in all three evaluations. Cumulatively, the four QTLs identified in this study explained 44, 60, and 68% of the variance in F2, and in F3 replications 1 and 2, respectively.
