Timing of Susceptibility to Fusarium Head Blight in Winter Wheat.

The duration of wheat susceptibility to Fusarium infection has implications for risk forecasting, fungicide timing, and the likelihood that visible kernel damage may underpredict deoxynivalenol (DON) contamination. A field experiment was conducted to explore the impact of varying infection timings on Fusarium head blight (FHB) development in winter wheat. Trials in four successive years (2010 to 2013) in North Carolina utilized one susceptible and one moderately resistant cultivar possessing similar maturity, stature, and grain quality. Inoculum was applied in the form of sprayed Fusarium graminearum conidia. In the first year, the nine infection timings were from 0 to 21 days after anthesis (daa), whereas in the following 3 years, they ranged from 0 to 13 daa. Infection progression was compared among inoculation timings by sampling spikes five to six times during grain-fill. Based on DON, percent kernel damage and kernel infection, and fungal spread as assayed via qPCR, the moderately resistant cultivar had at least a 2- to 3-day shorter window of susceptibility to damaging FHB infection than the susceptible cultivar. The results suggest that duration of susceptibility is an important aspect of cultivar resistance to FHB. In 2012, the window of susceptibility for both cultivars was extended by cold snaps during anthesis. After debranning in one year, the majority of DON was found to be in the bran fraction of kernels; there was also a trend for later infections to lead to a higher percentage of DON in the nonbran fraction, as well as a higher ratio of DON to FDK

Cephalosporium stripe of wheat : seedling-based resistance screening and pathogenic variability

Cephalosporium stripe of wheat (Triticum aestivum), caused by the soilborne fungus Cephalosporium gramineum, results in significant yield reductions in dryland winter wheat crops of the U.S. Pacific Northwest. The development of resistant cultivars offers the best hope for disease control. Breeding for resistance is hampered by the long trial times inherent in screening adult plants, and by cultivar x environment interactions in field tests. The principal objective of this research was to develop and test a procedure for screening wheat seedlings in controlled environments for resistance to Cephalosporium stripe. Wheat seedlings were raised hydroponically in growth chambers, and the fungus was increased in large fermentation tanks. The seedlings were inoculated at about 12 days post-germination. Disease severity was assessed approximately seven days later using a chlorophyll meter to measure the symptoms of chlorosis and striping. In three trials, five soft white cultivars from the Pacific Northwest and four hard red cultivars from the Southern Great Plains with known levels of field resistance were tested with a Pacific Northwest fungal isolate. With one exception, chlorophyll readings ordered the cultivars appropriately, with moderately resistant cultivars ranking above susceptible cultivars. Three other moderately resistant cultivars from the Pacific Northwest also appeared in one or two trials, and were ranked properly by chlorophyll level. Chlorophyll levels of uninoculated plants were assayed to determine if differences in chlorophyll content were innate in the cultivars. The chlorophyll levels of uninoculated and inoculated seedling treatments were only significantly correlated when the cultivar Madsen, which ranks high both in resistance and in chlorophyll content, was included. In adult plants, flag-leaf chlorophyll level corresponded to intensity of Cephalosporium stripe symptoms where disease was present, and was independent of known field resistance in undiseased cultivars. The seedling screening technique was used to investigate pathogenic variability in C. gramineum. In two experiments, a total of eight cultivars from the Pacific Northwest and the Southern Great Plains were tested with three fungal isolates from each region. No evidence of virulence/vertical resistance was found. There was also no significant adaptation of isolates to greater virulence on cultivars from the same region

Predicting Pre-planting Risk of Stagonospora nodorum blotch in Winter Wheat Using Machine Learning Models

Pre-planting factors have been associated with the late-season severity of Stagonospora nodorum blotch (SNB), caused by the fungal pathogen Parastagonospora nodorum, in winter wheat (Triticum aestivum). The relative importance of these factors in the risk of SNB has not been determined and this knowledge can facilitate disease management decisions prior to planting of the wheat crop. In this study, we examined the performance of multiple regression (MR) and three machine learning algorithms namely artificial neural networks, categorical and regression trees, and random forests (RF) in predicting the pre-planting risk of SNB in wheat. Pre-planting factors tested as potential predictor variables were cultivar resistance, latitude, longitude, previous crop, seeding rate, seed treatment, tillage type, and wheat residue. Disease severity assessed at the end of the growing season was used as the response variable. The models were developed using 431 disease cases (unique combinations of predictors) collected from 2012 to 2014 and these cases were randomly divided into training, validation, and test datasets. Models were evaluated based on the regression of observed against predicted severity values of SNB, sensitivity-specificity ROC analysis, and the Kappa statistic. A strong relationship was observed between late-season severity of SNB and specific pre-planting factors in which latitude, longitude, wheat residue, and cultivar resistance were the most important predictors. The MR model explained 33% of variability in the data, while machine learning models explained 47 to 79% of the total variability. Similarly, the MR model correctly classified 74% of the disease cases, while machine learning models correctly classified 81 to 83% of these cases. Results show that the RF algorithm, which explained 79% of the variability within the data, was the most accurate in predicting the risk of SNB, with an accuracy rate of 93%. The RF algorithm could allow early assessment of the risk of SNB, facilitating sound disease management decisions prior to planting of wheat

Pm223899, a new recessive powdery mildew resistance gene identified in Afghanistan landrace PI 223899

Key message A new recessive powdery mildew resistance gene, Pm223899, was identified in Afghanistan wheat landrace PI 223899 and mapped to an interval of about 831 Kb in the terminal region of the short arm of chromosome 1A. Abstract Wheat powdery mildew, a globally important disease caused by the biotrophic fungus Blumeria graminis f.sp. tritici (Bgt), has occurred with increased frequency and severity in recent years, and some widely deployed resistance genes have lost effectiveness. PI 223899 is an Afghanistan landrace exhibiting high resistance to Bgt isolates collected from the Great Plains. An F2 population and F2: 3 lines derived from a cross between PI 223899 and OK1059060-126135-3 were evaluated for response to Bgt isolate OKS(14)-B-3-1, and the bulked segregant analysis (BSA) approach was used to map the powdery mildew resistance gene. Genetic analysis indicated that a recessive gene, designated Pm223899, conferred powdery mildew resistance in PI 223899. Linkage analysis placed Pm223899 to an interval of about 831 Kb in the terminal region of chromosome 1AS, spanning 4,504,697–5,336,062 bp of the Chinese Spring reference sequence. Eight genes were predicted in this genomic region, including TraesCS1AG008300 encoding a putative disease resistance protein RGA4. Pm223899 was flanked proximally by a SSR marker STARS333 (1.4 cM) and distally by the Pm3 locus (0.3 cM). One F2 recombinant was identified between Pm3 and Pm223899 using a Pm3b-specific marker, indicating that Pm223899 is most likely a new gene, rather than an allele of the Pm3 locus. Pm223389 confers a high level of resistance to Bgt isolates collected from Pennsylvania, Oklahoma, Nebraska, and Montana. Therefore, Pm223389 can be used to enhance powdery mildew resistance in these states. Pm3b-1 and STARS333 have the potential to tag Pm223389 in wheat breeding

Explore the World with a Global Education Curriculum

Recognizing and celebrating the diversity that exists in our communities has become a central goal of land-grant institutions and cooperative extension programs. This is coupled with the expectation that youth be equipped for a global workforce where they appreciate different world cultures, be able to evaluate global issues and challenges and understand the inter-connectedness of global systems. Given these points, a Global Education Curriculum developed by the WVU Extension Global Education & Engagement Team is presented as a tool to instill a deeper understanding of and appreciation for cultures, people and global issues by youth and the adults who support them

Explore the World with a Global Education Curriculum

Recognizing and celebrating the diversity that exists in our communities has become a central goal of land-grant institutions and cooperative extension programs. This is coupled with the expectation that youth be equipped for a global workforce where they appreciate different world cultures, be able to evaluate global issues and challenges and understand the inter-connectedness of global systems. Given these points, a Global Education Curriculum developed by the WVU Extension Global Education & Engagement Team is presented as a tool to instill a deeper understanding of and appreciation for cultures, people and global issues by youth and the adults who support them

Global genomic analyses of wheat powdery mildew reveal association of pathogen spread with historical human migration and trade

The fungus Blumeria graminis f. sp. tritici causes wheat powdery mildew disease. Here, we study its spread and evolution by analyzing a global sample of 172 mildew genomes. Our analyses show that B.g. tritici emerged in the Fertile Crescent during wheat domestication. After it spread throughout Eurasia, colonization brought it to America, where it hybridized with unknown grass mildew species. Recent trade brought USA strains to Japan, and European strains to China. In both places, they hybridized with local ancestral strains. Thus, although mildew spreads by wind regionally, our results indicate that humans drove its global spread throughout history and that mildew rapidly evolved through hybridization.Centro de Investigaciones AgropecuariasFil: Sotiropoulos, Alexandros G. University of Zurich. Department of Plant and Microbial Biology; SuizaFil: Arango-Isaza, Epifanía. University of Zurich. Department of Evolutionary Biology and Environmental Studies; SuizaFil: Ban, Tomohiro. Yokohama City University. Kihara Institute for Biological Research; JapónFil: Barbieri, Chiara. University of Zurich. Department of Evolutionary Biology and Environmental Studies; SuizaFil: Barbieri, Chiara. Max Planck Institute for Evolutionary Anthropology. Department of Linguistic and Cultural Evolution; AlemaniaFil: Bourras, Salim. University of Zurich. Department of Plant and Microbial Biology; SuizaFil: Bourras, Salim. University of Agricultural Sciences. Department of Forest Mycology and Plant Pathology; SueciaFil: Cowger, Christina. North Carolina State University; Estados Unidos. USDA-ARS Department of Plant Pathology; Estados UnidosFil: Czembor, Paweł C. National Research Institute. Plant Breeding and Acclimatization Institute; PoloniaFil: Ben-David, Roi. ARO-Volcani Center. Institute of Plant Sciences. Department of Vegetables and Field Crops; IsraelFil: Dinoor, Amos. University of Jerusalem. The Robert H. Smith Faculty of Agriculture, Food & Environment. Department of Plant Pathology and Microbiology; IsraelFil: Ellwood, Simon R. Curtin University. School of Molecular and Life Sciences. Centre for Crop and Disease Management; AustraliaFil: Graf, Johannes. University of Zurich. Department of Plant and Microbial Biology; SuizaFil: Hatta, Koichi. National Agricultural Research Organization. Hokkaido Agricultural Research Center Field Crop Research and Development; JapónFil: Helguera, Marcelo. Instituto Nacional de Tecnología Agropecuaria (INTA). Centro de Investigaciones Agropecuarias; ArgentinaFil: Wicker, Thomas. University of Zurich. Department of Plant and Microbial Biology; Suiz

Global genomic analyses of wheat powdery mildew reveal association of pathogen spread with historical human migration and trade

The fungus Blumeria graminis f. sp. tritici causes wheat powdery mildew disease. Here, Sotiropoulos et al. analyze a global sample of 172 mildew genomes, providing evidence that humans drove global spread of the pathogen throughout history and that mildew rapidly evolved through hybridization with local fungal strains.The fungus Blumeria graminis f. sp. tritici causes wheat powdery mildew disease. Here, we study its spread and evolution by analyzing a global sample of 172 mildew genomes. Our analyses show that B.g. tritici emerged in the Fertile Crescent during wheat domestication. After it spread throughout Eurasia, colonization brought it to America, where it hybridized with unknown grass mildew species. Recent trade brought USA strains to Japan, and European strains to China. In both places, they hybridized with local ancestral strains. Thus, although mildew spreads by wind regionally, our results indicate that humans drove its global spread throughout history and that mildew rapidly evolved through hybridization

Effects of host resistance on Mycosphaerella graminicola populations

Mycosphaerella graminicola (anamorph Septoria tritici) causes Septoria tritici blotch, a globally important disease of winter wheat. Resistance and pathogenicity generally vary quantitatively. The pathogen reproduces both sexually and asexually, and the pathogen population is highly genetically variable. Several unresolved questions about the epidemiology of this pathosystem are addressed by this research. Among them are whether cultivar-isolate specificity exists, how partial host resistance affects pathogen aggressiveness and sexual reproduction, and how host genotype mixtures influence epidemic progression and pathogenicity. At its release in 1992, the cultivar Gene was highly resistant to M. graminicola, but that resistance had substantially dissolved by 1995. Six of seven isolates collected in 1997 from field plots of Gene were virulent to Gene seedlings in the greenhouse, while 14 of 15 isolates collected from two other cultivars were avirulent to Gene. Gene apparently selected for strains of M. graminicola with specific virulence to it. In a two-year experiment, isolates were collected early and late in the growing season from field plots of three moderately resistant and three susceptible cultivars, and tested on seedlings of the same cultivars in the greenhouse. Isolates were also collected from plots of two susceptible cultivars sprayed with a fungicide to suppress epidemic development. Isolate populations were more aggressive when derived from moderately resistant than from susceptible cultivars, and more aggressive from fungicide-sprayed plots than from unsprayed plots of the same cultivars. Over 5,000 fruiting bodies were collected in three years from replicated field plots of eight cultivars with different levels of resistance. The fruiting bodies were identified as M. graminicola ascocarps or pycnidia, or other. In all three years, the frequency of ascocarps was positively correlated with cultivar susceptibility, as measured by area under the disease progress curve, and was also positively associated with epidemic intensity. For three years, four 1:1 mixtures of a moderately resistant and a susceptible wheat cultivar were planted in replicated field plots. Isolates from the plots were inoculated as bulked populations on greenhouse-grown seedlings of the same four cultivars. Mixture effects on disease progression varied among the years, and were moderately correlated with mixture effects on pathogenicity