Powdery mildew is a major fungal disease in wheat growing areas worldwide. A novel source of resistance to wheat powdery mildew present in the germplasm line NC97BGTD7 was genetically characterized as a monogenic trait in greenhouse and field trials using F(2) derived lines from a NC97BGTD7 X Saluda cross. Microsatellite markers were used to map and tag this resistance gene, now designated Pm34. Three co-dominant microsatellite markers linked to Pm34 were identified and their most likely order was established as: Xbarc177-5D, 5.4cM, Pm34, 2.6cM, Xbarc144-5D, 14cM, Xgwm272-5D. These microsatellite markers were previously mapped to the long arm of the 5D chromosome and their positions were confirmed using Chinese Spring nullitetrasomic Nulli5D-tetra5A and ditelosomic Dt5DL lines. Pm2, the only other known Pm gene on chromosome 5D, has been mapped to the short arm and its specificity is different from that of Pm34.

A single gene controlling powdery mildew resistance was identified in the North Carolina germplasm line NC96BGTD3 (NCD3) using genetic analysis of F(2) derived lines from a NCD3 X Saluda cross. Microsatellite markers linked to this Pm gene were identified and their most likely order was Xcfd7, 10.3 cM, Xgdm43, 8.6 cM, Xcfd26, 11.9 cM, Pm gene. These markers and the Pm gene were assigned to chromosome 5DL by means of Chinese Spring Nullitetrasomic (Nulli5D-tetra5A) and ditelosomic (Dt5DL) lines. A detached leaf test showed a distinctive disease reaction to six pathogen isolates among the NCD3 Pm gene, Pm2 (5DS) and Pm34 (5DL). An allelism test showed independence between Pm34 and the NCD3 Pm gene. Together, the tests provided strong evidence for the presence of a novel Pm gene in NCD3, and this gene was designated Pm35.

Changes in milling and baking quality (especially flour yield) of soft red winter wheat can have a large economic impact on flour mills. To determine the relationship between early-season powdery mildew and late-season leaf rust on flour yield, flour protein, alkaline water retention capacity, and kernel texture (softness equivalent), a study was conducted over 2 years at Kinston and Plymouth, NC. Different levels of powdery mildew and leaf rust developed on three winter wheat cultivars that varied in levels of disease resistance, the presence of seed treatment, and the presence and timing of foliar fungicide application. In Kinston and Plymouth in 1989-90, where leaf rust occurred early, the softness equivalent score was lower in wheat grown from seed treated with triadimenol. The following year, when the leaf rust epidemic increased later, foliar fungicide application reduced disease and resulted in lower softness equivalent scores in both Plymouth and Kinston for cv. Saluda and in Kinston for cv. Coker 983. A regression model was developed to describe the relationship between the log of the area under the disease progress curves and adjusted flour yield (AFY). The AFY of Saluda was reduced in the presence of powdery mildew such that %AFY = 103.96 - 0.92 (log AUMPC).

A major gene for resistance to wheat powdery mildew (Blumeria graminis f. sp. tritici = Erysiphe graminis f. sp. tritici) has been successfully transferred into hexaploid common wheat (Triticum aestivum, 2n = 6x = 42, AABBDD) from wild einkorn wheat (Triticum monococcum subsp. aegilopoides, 2n = 2x = 14, AA). NC96BGTA5 is a germ plasm line with the pedigree Saluda x 3/PI427662. The response patterns for powdery mildew resistance in NC96BGTA5 were tested with 30 differential isolates of B. graminis f. sp. tritici, and the line was resistant to all tested isolates. The analyses of P(1), P(2), F(1), F(2), and BC(1)F(1) populations derived from NC96BGTA5 revealed two genes for wheat powdery mildew resistance in the NC96BGTA5 line. One gene, Pm3a, was from its recurrent parent Saluda, and the second was a new gene introgressed from wild einkorn wheat. The gene was determined to be different from Pm1 to Pm21 by gene-for-gene and pedigree analyses. The new gene was identified as linked to the Pm3a gene based on the F(2) and BC(1)F(1) populations derived from a cross between NC96BGTA5 and a susceptible cultivar NK-Coker 68-15, and the data indicated that the gene was located on chromosome 1A. It is proposed that this new gene be designated Pm25 for wheat powdery mildew resistance in NC96BGTA5. Three random amplified polymorphic DNA markers, OPX06(1050), OPAG04(950), and OPAI14(600), were found to be linked to this new gene.

Fusarium head blight (FHB) can reduce yield of wheat and decrease the value of harvested grain by accumulation of detrimental toxins. Understanding the variability of the fungal population associated with infection could improve disease control strategies. Sixty-six isolates of Fusarium graminearum associated with FHB were collected in North Carolina and tested for in vitro growth rate, in vitro production of deoxynivalenol (DON) and zearalenone, and pathogenicity on three cultivars of soft red winter wheat. Significant differences among isolates were found for all three traits. Randomly Amplified Polymorphic DNA (RAPD) analysis revealed high levels of genotypic diversity among isolates. Isolates of F. graminearum, F. culmorum, and F. avenaceum acquired from the Pennsylvania State University Fusarium Center were included for comparison in all tests. In vivo levels of DON were measured for the five isolates associated with the highest levels of disease and the five isolates associated with the lowest levels of disease, and no significant differences were found. However, all ten isolates produced detectable levels of DON in vivo. Mean disease ratings ranged from 3.4 to 96.4%, in vitro (DON) levels ranged from 0 to 7176.2 ppm, and zearalenone ranged from 0 to 354.7 ppm, among isolates. A multiple regression model using in vitro growth, in vitro DON, and zearalenone production, collection location, wheat cultivar of isolate origin, plot, tillage conditions, and previous crop as independent variables and percent blighted tissue as the dependent variable was developed. The cumulative R2 value for the model equaled 0.27 with in vitro rate of growth making the largest contribution. Analysis of phenotype and genotype among isolates demonstrated diversity in a single plot, in a single location, and in North Carolina. Genotypic and phenotypic diversity were significant under both conventional and reduced tillage conditions, and diversity was high regardless of whether the previous crop had been a host or non-host for F. graminearum. These data indicate a variable pathogen population of F. graminearum exists in North Carolina, and members of this population can be both highly pathogenic on wheat and produce high levels of detrimental toxins, indicating a potential threat for problems with FHB within the state.

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Samples of perithecia of Blumeria graminis f. sp. tritici from senescing wheat leaves were collected by cooperators from 17 states. Ascospores were discharged from perithecia and single-spore isolates were characterized for virulence genes using a differential host series containing 15 known resistance genes. A total of 520 isolates from 17 states were characterized in 1993 and 1994. Virulence frequencies and complexity and racial composition were examined. The data were analyzed for associations among sets of virulence genes and the geographical distribution of phenotypes. Virulence to Pm3c, Pm3f, pm5, Pm6, and Pm7 was present in all states surveyed. Since 1990, virulence to Pm3a has increased in the northeast, and virulence to Pm1, Pm4b, Pm8, and Pm17 has increased across the area surveyed. The resistance genes Pm12 and Pm16 remain highly effective in the southeastern United States. An increase in virulence frequencies and complexity of isolates was observed.

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